50 results about "Malignant progression" patented technology

The invention provides computer equipment for executing a sub-solid pulmonary nodule growth prediction method based on CT imageomics, and the computer equipment comprises a memory, a processor and a computer program, and when the processor executes the program, density value extraction is carried out on a sub-solid pulmonary nodule region through multi-stage CT images, the internal structure of a nodule is segmented by adopting a convolutional neural network, and the internal structure of the nodule is obtained; obtaining nodule internal density distribution data from the segmentation result; calculating a cavity expansion rate and an edge density increase rate in unit time by combining the density amplitude data according to a focus characteristic influence degree evaluation result; according to the lesion cavity expansion rate and the edge density growth rate, the malignant progress risk level is judged, and malignant progress time window estimation is obtained; according to the malignant progress time window estimation, the matching degree between the density distribution data and the development speed index is calibrated through clinical feedback data, and sub-solid pulmonary nodule growth prediction output is obtained.

The invention discloses application of a palmitoylation inhibitor in prevention and treatment of gastric cancer. The chromatin remodeling protein SNF2 derived from S.anginosus EVs can be combined with a transcription factor TEAD1, so that the transcription of the palmitoyl transferase ZDHHC11 is promoted together. Then, the stability of the ZDHHC11 is enhanced by catalyzing palmitoylation of PD-L1, and finally immune escape is induced. In addition, SNF2 also can activate AXL, CTGF, CYR61 and other carcinogenic targets at the downstream of TEAD1, thereby further accelerating the malignant progression of gastric cancer. In an in-vivo experiment, the intragastric administration of the S.anginosus EVs not only promotes the tumor growth of mice, but also significantly inhibits the infiltration of CD8 + T cells. Blocking of ZDHHC11 can effectively reverse immune escape, and has a synergistic effect with an anti-PD-1 therapy, so that the treatment effect is remarkably improved.

The invention discloses an application of COX4I2 in preparation of a non-small cell lung cancer medicine. Specifically, the invention also discloses an application of COX4I2 in preparation of a mitochondrial iron overload preparation and an application of a COX4I2 gene inhibitor in preparation of a preparation for promoting malignant progression of tumors. According to the invention, a COX4I2-VDAC1 interaction inhibitor is screened, a COX4I2 degradation agent or cluster-competitive peptide is developed, a brand new combined chemotherapy regimen is provided for solid tumors such as NSCLC and the like, and the polypeptide has the potential of expanding to cluster metabolic disorder diseases such as neurodegenerative diseases and diabetes mellitus.

The invention discloses an application of SNF2 protein derived from streptococcus angina extracellular vesicles in gastric cancer prognosis. The chromatin remodeling protein SNF2 derived from S.anginosus EVs can be combined with a transcription factor TEAD1, so that the transcription of the palmitoyl transferase ZDHHC11 is promoted together. Then, the stability of the ZDHHC11 is enhanced by catalyzing palmitoylation of PD-L1, and finally immune escape is induced. In addition, SNF2 also can activate AXL, CTGF, CYR61 and other carcinogenic targets at the downstream of TEAD1, thereby further accelerating the malignant progression of gastric cancer. In an in-vivo experiment, the intragastric administration of the S.anginosus EVs not only promotes the tumor growth of mice, but also significantly inhibits the infiltration of CD8 + T cells. Blocking of ZDHHC11 can effectively reverse immune escape, and has a synergistic effect with an anti-PD-1 therapy, so that the treatment effect is remarkably improved.

This invention discloses the application of ESCO1 and NUFIP2 in the diagnosis and treatment of pancreatic cancer, relating to the field of biomedical technology. This invention provides the application of ESCO1 and / or NUFIP2 as pancreatic cancer biomarkers in the preparation of pancreatic cancer diagnostic or prognostic assessment products, and also provides the application of ESCO1 and / or NUFIP2 as drug targets in the screening or preparation of drugs for the prevention and / or treatment of pancreatic cancer. This invention discovers that ESCO1 and NUFIP2 have important biological significance in pancreatic cancer, with NUFIP2 expression regulated by ESCO1, and both expression levels positively correlated with the malignant progression of pancreatic cancer. Therefore, ESCO1 and NUFIP2 can not only serve as potential diagnostic biomarkers and therapeutic targets for pancreatic cancer, but also provide new theoretical basis and research directions for optimizing pancreatic cancer immunotherapy strategies.

The invention provides a synergistic treatment pharmaceutical composition for preventing and treating recurrence after hepatocellular carcinoma thermal ablation and application of the synergistic treatment pharmaceutical composition. Aiming at malignant tumor progression driven by ACSS3 gene silencing after thermal ablation, an epigenetic editing technology is innovatively combined with metabolite supplementation, and a preparation for specifically activating or promoting ACSS3 gene expression and sodium propionate are cooperatively used, so that ACSS3 can be remarkably reactivated or expression can be promoted in a xenograft model derived from a cell line and a patient; the compound can be used for recovering propionyl-coenzyme A synthesis and normal propionic acid metabolism and inhibiting fatty acid beta-oxidation, so that the growth and metastasis of post-ablation hepatocellular carcinoma (HCC) are effectively blocked, and the limitation of a single therapy is overcome. A clearer mechanism target is provided for preventing recurrence after HCC thermal ablation, meanwhile, the prepared targeting nano-liposome preparation has a synergistic effect, and as a brand-new treatment strategy, the defect that intervention on recurrence roots is insufficient in the prior art is overcome.

The application discloses application of CPSF7 as an ovarian cancer treatment and prognosis target, and relates to the technical field of biological medicine.The application research finds that overexpression of CPSF7 is related to poor prognosis of ovarian cancer, indicating that CPSF7 can be used as a prognosis index and potential treatment target of ovarian cancer.Further research shows that CPSF7 promotes malignant progression of ovarian cancer by promoting proliferation, migration and invasion of ovarian cancer cells, and inhibition of CPSF7 expression can significantly inhibit proliferation, migration and invasion of ovarian cancer cells.The application also finds that UBE2K is one of key downstream targets of CPSF7 in the ovarian cancer cell-mediated carcinogenic process, and inhibition of UBE2K expression can weaken the overexpression of CPSF7 induced enhancement effect of ovarian cancer cell proliferation, migration and invasion.The application provides a new target for treatment and prognosis prediction of ovarian cancer, and has important clinical application value.

The application provides application of MTA1 which is highly expressed in glioma stem cells (GSC) in treatment of glioblastoma (GBM). The application firstly proposes that GSC in GBM highly expresses MTA1 protein molecules, the highly expressed MTA1 is positively correlated with poor prognosis of GBM patients, and also promotes the stemness, cell proliferation and spheroid formation ability of GSC. Targeting the highly expressed MTA1 in GSC can inhibit the malignant progression of GBM. The application provides a new target and inhibitor for targeted treatment of GBM.

The application discloses an intervention strategy for targeting CACNA2D2 protein and application thereof, and belongs to the technical field of medicine and biotechnology.The application discloses for the first time that abnormal high expression of CACNA2D2 is related to poor prognosis of neuroblastoma, especially malignant progression, and provides that CACNA2D2 gene is used as a drug target to prepare a drug for treating neuroblastoma, and further provides application of CACNA2D2 siRNA in preparation of a drug for treating neuroblastoma.After down-regulation of CACNA2D2 gene expression, cell proliferation and clone formation ability of neuroblastoma cells are significantly inhibited.Therefore, the application provides a new direction for development of a drug for treating neuroblastoma, and provides a possibility for preparing a new drug for treating neuroblastoma, improving curative effect of patients, improving prognosis and survival.

This invention discloses DLL3 as a therapeutic target for cervical neuroendocrine carcinoma and its application, belonging to the field of biotechnology. This invention discloses the specific expression of the DLL3 gene in cervical neuroendocrine carcinoma (NECC) and its application as a therapeutic target. Single-cell sequencing and immunohistochemistry revealed activation of the DLL3-NOTCH1 / 2 signaling axis in NECC, and functional experiments confirmed that it drives malignant progression by promoting tumor proliferation and inducing T cell exhaustion. Furthermore, this invention constructed an NECC organoid-TIL co-culture model to verify the synergistic efficacy of the DLL3-targeting drug AMG757 combined with EP chemotherapy. This invention provides new target selection and theoretical basis for the precision diagnosis and treatment of NECC, and has significant clinical translational value.

The invention provides preparation and application of a kidney dual-targeting black phosphorus nano platform for treating acute kidney injury. Firstly, black phosphorus nanosheets and NH2-PEG-NH2 are mixed and then dispersed into deionized water, centrifugation is repeated, supernate is discarded, and a BP-PEG solution is obtained; kim-1 targeted polypeptide LTH powder is dissolved in deionized water, then EDC and NHS are added for a light-shielding reaction, a BP-PEG solution is added, light-shielding stirring is continued to obtain a BP-PEG-LTH mixture, then 4-octyl itaconic acid is added, then a PBS solution is added, light-shielding magnetic stirring is carried out, and the kidney double-targeting black phosphorus nano platform is obtained. The kidney dual-targeting black phosphorus nano platform is used as an intravenous injection for treating acute kidney injury, oxidative stress can be rapidly and effectively inhibited, inflammation is resisted, intercellular burial is promoted, malignant development of AKI is inhibited to a great extent, and the purpose of short-term specific intervention treatment after AKI is achieved.

The application discloses poplar phellinus polysaccharide SVP-1, a preparation method and application thereof, and belongs to the field of biological medicines. The poplar phellinus polysaccharide SVP-1 provided by the application has significant antitumor activity, can effectively inhibit the proliferation, invasion and migration of tumor cells, and thus blocks the malignant progression of tumors. The structure is clear, the preparation method is controllable, the stability and biological activity of the polysaccharide component are ensured, and a reliable foundation is provided for the development of antitumor drugs. The combination with radiotherapy and chemotherapy drugs can play a synergistic effect, can not only improve the sensitivity of tumors to treatment, but also reduce the toxic and side effects of radiotherapy and chemotherapy, and realizes the effect of 'attenuation and synergism'. The combined treatment strategy can significantly improve the curative effect of the existing tumor therapy, while reducing the adverse reactions, and provides a new optimization scheme for clinical tumor treatment.

This invention discloses the application of the CEMIP-ITGA5 axis as a target in the preparation of products that regulate epithelial-mesenchymal transition (EMT) and metastasis in lung adenocarcinoma, belonging to the fields of tumor molecular biology and precision medicine. Through TCGA-LUAD cohort bioinformatics analysis, immunohistochemical verification of clinical specimens, cell function experiments, and a nude mouse subcutaneous xenograft model, this invention discovers and confirms that the CEMIP-ITGA5 axis participates in regulating epithelial-mesenchymal transition, migration, invasion, and metastasis-related malignant progression in lung adenocarcinoma. Specifically, CEMIP positively regulates ITGA5 expression, thereby promoting EMT, proliferation, migration, invasion, and in vivo tumorigenesis in lung adenocarcinoma cells. Based on this, the present invention provides two applications: Firstly, by detecting the expression levels of the dual genes CEMIP and ITGA5, a kit for assessing the risk of epithelial-mesenchymal transition (EMT) and metastasis in lung adenocarcinoma can be prepared. The combined detection of CEMIP and ITGA5 can reflect the activation status of the CEMIP-ITGA5 axis at both the upstream regulatory molecule and downstream effector molecule levels, providing auxiliary molecular evidence for assessing EMT and metastasis-related risks in lung adenocarcinoma. Secondly, by targeting and inhibiting the expression or function of CEMIP and / or ITGA5, drugs can be prepared to inhibit epithelial-mesenchymal transition, migration, invasion, and metastasis-related malignant progression in lung adenocarcinoma, effectively reversing the epithelial-mesenchymal transition phenotype and inhibiting tumor malignant progression. This invention provides novel molecular targets and technical solutions independent of known signaling pathways for prognostic assessment and targeted therapy of lung adenocarcinoma.

The invention relates to the technical field of biological medicine, and particularly discloses application of nefenavir. Nefinavir is used for preparing a medicine for treating or preventing castration-resistant prostate cancer, and the medicine can specifically up-regulate expression of DHCR7, induce DNA damage of tumor cells and activate a cell cycle arrest pathway mediated by periodic protein of the cells so as to inhibit key biological processes such as proliferation of the tumor cells, cholesterol metabolism and the like; especially, formation and amplification of multinuclear giant cells in castration-resistant prostate cancer can be effectively inhibited by up-regulating expression of DHCR7, so that malignant progression of multinuclear giant cell mediated tumors and treatment of drug resistance are blocked. Finally, the castration-resistant prostate cancer is prevented and treated, and the technical bottlenecks that an existing castration-resistant prostate cancer treatment means is limited in curative effect, and the drug resistance and metastasis capability mediated by multinuclear giant cells are difficult to inhibit in a targeted manner are solved.

This invention discloses the application of SDC1 in the diagnosis and treatment of breast cancer. Through bioinformatics analysis, cell function experiments, multi-omics analysis, and animal model validation, this invention reveals for the first time the high expression of SDC1 in breast cancer and its correlation with poor patient prognosis. It elucidates the molecular mechanism by which SDC1 promotes the malignant progression of breast cancer by regulating ECM remodeling, EMT, angiogenesis, and ferroptosis resistance, and verifies the therapeutic potential of MZ1 in inhibiting breast cancer growth and metastasis by downregulating SDC1 expression. This invention provides the application of reagents for detecting SDC1 expression levels in the preparation of diagnostic or prognostic kits for breast cancer, as well as the application of SDC1 inhibitors in the preparation of drugs for treating breast cancer. This invention provides new technical solutions for the diagnosis, prognostic assessment, and treatment of breast cancer.

The invention discloses application of MYSM1 regulation and control of ITPR1 mediated cell autophagy in inhibition of cervical cancer, and belongs to the technical field of biomedicine.The MYSM1 gene and / or expression or activity of encoded protein of the MYSM1 gene are / is up-regulated, and an MYSM1-ITPR1-autophagy signal channel is activated, so that proliferation, migration, invasion or epithelial-mesenchymal transition of cervical cancer cells is inhibited, and cervical cancer is inhibited. And / or promoting apoptosis of cervical cancer cells; wherein the MYSM1 activates the expression of ITPR1 through the activity of a deubiquitination enzyme which is subjected to single ubiquitination modification on the 119th lysine of histone H2A of the MYSM1, and the ITPR1 serves as an endoplasmic reticulum calcium ion channel to mediate calcium ion release so as to trigger cell autophagy. Based on the mechanism, the invention provides a new application of MYSM1 / ITPR1 in preparation of anti-cervical cancer drugs, a drug composition targeting the pathway, a candidate drug screening method and a kit for diagnosis and prognosis. The invention aims to solve the problem that a technical scheme for effectively inhibiting the malignant progression of cervical cancer by targeting an MYSM1-ITPR1 pathway is lacked in the prior art.

The invention discloses a biomarker for predicting prognosis of esophageal squamous carcinoma and application of the biomarker, and relates to the technical field of biological medicines. The biomarker is tRF-24, and the nucleotide sequence of the biomarker is as shown in SEQ ID NO. 1. Researches find that the expression of tRF-24 in esophageal squamous cell carcinoma tumor tissues is obviously higher than that in para-carcinoma normal tissues, the expression quantity of late patients is obviously higher than that of early patients, and the higher the expression level is, the shorter the total lifetime of the patients is, and the poorer the prognosis is. Due to the characteristics, the tRF-24 can be used as one of important indexes for judging the clinical outcome of the esophageal squamous carcinoma patient. The invention proves that malignant progression of esophageal squamous carcinoma can be inhibited by reducing the expression quantity of tRF-24, which provides solid theoretical support and experimental basis for targeted therapy of tRF-24.

This invention discloses a biomimetic exosome system and method for producing a glucose metabolism-based glycosidase for the treatment of fatty liver-associated hepatocellular carcinoma, which involves transfecting mesenchymal stem cells with a glycosidase sequence by lentiviral transfection, followed by obtaining exosomes by ultracentrifugation. The biomimetic exosome system of this invention possesses target migration ability, low immunogenicity, improved ability to transport bioactive substances, normalizes disrupted glucose metabolism, reduces endoplasmic reticulum stress, and suppresses epithelial-mesenchymal transition signaling. Both in vivo and in vitro experiments have verified that it can effectively target cancer cells in vivo, reduce abnormal O-GlcNAc modifications, and inhibit tumor malignancy, and after reaching fatty liver-associated hepatocellular carcinoma in vivo, it can reduce O-GlcNAc modification levels, restore disrupted metabolism, and suppress cancer progression.

The invention discloses an application of TCF7L2 (T cell factor 7L2) in treatment of glioblastoma. The research shows that the transcription factor TCF7L2 has an important tumor inhibition effect in glioblastoma cells (GBM), and the deletion of the transcription factor TCF7L2 can obviously accelerate the growth and malignant progression of tumor cells, so that the response capability of the GBM cells to exogenous neural signals is enhanced, and the tumor development is further promoted. In mechanism, the TCF7L2 regulates and controls the expression of various neurotransmitter receptors, and inhibitors applying the receptors can effectively reverse tumor promoting phenotypes caused by deletion of the TCF7L2, so that the TCF7L2 plays a key role in inhibiting GBM nerve dependence progression by maintaining the steady state of neural signal related receptors. The invention provides a new diagnostic and prognostic marker and a new therapeutic target for treatment of GBM, and provides a new thought and a new strategy for treatment of GBM.

The invention relates to the technical field of biological medicines, in particular to application of a Metrnl gene in preparation of a medicine for treating tumors. A series of experiments prove that metrnl overexpression can significantly promote proliferation, migration and invasion of liver cancer cells, and targeted inhibition of expression or activity of metrnl can block malignant progression of liver cancer. Meanwhile, by performing associated signal analysis on expression characteristics and prognosis of the Metrnl in various tumors, the effectiveness and feasibility of the Metrnl gene as a treatment target of various tumors such as ovarian cancer, lung adenocarcinoma and the like are verified. The invention provides therapeutic targets for various tumors (especially lung cancer), provides technical support for research and development of related tumor therapeutic drugs, and has important clinical application value.

The invention discloses application of circZFAND6 as a target spot in preparation of a product for treating ovarian cancer, and belongs to the technical field of biological medicine. The invention discloses a key action mechanism of circZFAND6 derived from TAMs exosome in the occurrence and development of the ovarian cancer. After the exosome circZFAND6 secreted by the TAMs is over-expressed and is taken by the ovarian cancer cells, the proliferation, migration and invasion capabilities of the cancer cells can be remarkably promoted; knock-down can effectively inhibit the malignant biological behaviors. According to the circZFAND6, the stability of c-Myc protein is maintained, glycolysis key enzyme expression regulated and controlled by c-Myc is up-regulated, the Warburg effect is enhanced, and the malignant progression of ovarian cancer is accelerated. The invention not only provides a solid theoretical basis and experimental evidence for the therapy strategy of the targeted circZFAND6 ovarian cancer, but also opens up a new direction for the intervention research of tumor metabolism reprogramming.

The invention discloses a cervical cancer influence mechanism research method based on ICAT regulated ferroptosis, and relates to the technical field of molecular biology. Comprising the following steps: evaluating the ferroptosis effect of ICAT in cervical cancer; the ICAT is verified to promote the malignant progression of cervical cancer by inhibiting ferroptosis; the molecular mechanism of ICAT for inhibiting cervical cancer ferroptosis is clarified; and screening an anti-cervical cancer candidate compound. According to the invention, the action downstream target of ICAT is accurately positioned as GPX4 through proteomics and immunoprecipitation-mass spectrometry, and the specific mechanism of stabilizing GPX4 protein by influencing ZDHHC5-mediated palmitoylation is clarified, so that the target is very clear; a targeted drug screening strategy is designed for screening small molecule compounds, antibodies or nucleic acid drugs capable of targeting ICAT or destroying GPX4 palmitoylation, and a clear target spot and a feasible screening path are provided for developing novel anti-cervical cancer drugs.

The invention discloses a traditional Chinese medicine composition and application thereof in preparation of medicines for treating gastric precancerous lesions and inhibiting gastritis-cancer transformation. The traditional Chinese medicine composition is prepared from astragalus membranaceus, red ginseng, pseudo-ginseng, pericarpium citri reticulatae, bran-fried rhizoma atractylodis macrocephalae, rhizoma zingiberis, rhizoma pinelliae preparata, rhizoma coptidis, ovateleaf holly bark and honey-fried licorice root. The traditional Chinese medicine composition provided by the invention is good in safety, has double curative effects, not only can repair gastric mucosa injury, relieve inflammation, inhibit epithelial cell-mesenchymal transformation of gastric mucosa, improve gastric mucosa tissue lesion and block gastric'inflammation-cancer 'transformation, but also has a direct anti-gastric cancer effect, can inhibit invasion and metastasis of gastric cancer and promote apoptosis of gastric cancer cells, and has the effects of preventing and treating gastric cancer. A new drug choice is provided for blocking and reversing the malignant progress of gastric mucosa in a safe and effective traditional Chinese medicine within a stomach'inflammation-cancer 'time window, and the application prospect is wide.

The application discloses application of hnRNPL in preparation of glioma diagnosis, treatment and prognosis evaluation products, and belongs to the technical field of biological medicine. Through bioinformatics and clinical sample verification, it is confirmed that hnRNPL is significantly highly expressed in glioma tissues, and the expression level thereof is negatively correlated with the total survival period of patients, and hnRNPL has the function of promoting the occurrence and development of glioma. Mechanism research shows that hnRNPL can be used as a key alternative splicing factor, which promotes the skipping of the second exon of SH3BGRL by combining with the CA-rich sequence on the SH3BGRL pre-mRNA, thereby generating functional SH3BGRL protein, and driving the proliferation, migration and invasion of glioma cells. Based on this, hnRNPL can be used as a molecular marker for the diagnosis and prognosis evaluation of glioma, and an inhibitor targeting hnRNPL can effectively inhibit the malignant progression of glioma.

This invention relates to the field of biomedical technology, and discloses the application of NAT10 inhibitors in the preparation of drugs for treating intrahepatic cholangiocarcinoma. This invention reveals for the first time that N-acetyltransferase 10 (NAT10) catalyzes the N-acetyltransferase in CHAF1A mRNA... 4 - Acetylcytidine (ac) 4 C) Modification enhances its stability and upregulates the expression of chromatin assembly factor CHAF1A. CHAF1A inhibits the transcription of the transposon element HERV9NC-int through epigenetic mechanisms, reducing the accumulation of intracellular double-stranded RNA (dsRNA), thereby weakening the innate immune response of tumor cells, promoting immune escape, and driving the malignant progression of intrahepatic cholangiocarcinoma. Inhibiting NAT10 expression or activity can effectively block this oncogenic pathway, significantly inhibiting ICC cell proliferation and migration, and enhancing the anti-tumor immune response. This invention provides a new molecular target and therapeutic strategy for the treatment of intrahepatic cholangiocarcinoma.

The invention belongs to the field of biological medicine, and particularly relates to application of a targeted JOSD1 inhibitor in preparation of tumor treatment drugs. Researches find that deubiquitinating enzyme JOSD1 is highly expressed in HCC and is closely related to poor prognosis of a patient. The JOSD1 stabilizes PGAM1 protein on a key lysine site by regulating ubiquitination-lactic acid post-modification (PTM) interaction of a glycolysis key enzyme PGAM1, enhances the enzymatic activity and lactic acid generation of the PGAM1 protein, and promotes glycolysis metabolism and malignant progression of tumor cells. The accumulation of lactic acid causes infiltration and function inhibition of CD8T cells, so that an immunosuppressive tumor microenvironment is formed. Targeted inhibition of JOSD1 can significantly reduce the proliferation and transfer ability of HCC cells and recover immune response. Animal experiments show that the liver-specific JOSD1 inhibitor can effectively inhibit tumor progression and has a remarkable synergistic effect with anti-PD-1 immunotherapy, and the lifetime is prolonged.

The invention relates to a natural active polypeptide capable of being used for tissue regeneration, beauty, health care and cancer resistance and application of the natural active polypeptide, and the amino acid sequence of the active polypeptide is shown as SEQ ID No.1, specifically MARSPSGPFTPVPTAT. The polypeptide can promote the proliferation of fibroblasts and skin keratinocytes, and can be used as a therapeutic agent for clinically promoting wound healing; oxygen free radicals can be efficiently removed, and the antioxidant activity is remarkable; the expression of the polypeptide provided by the invention is up-regulated in pancreatic cancer, and malignant progression of pancreatic cancer can be promoted through the ORF2 encoded polypeptide. Therefore, the polypeptide disclosed by the invention can be widely applied to related products such as biological medicine, regenerative medicine, tissue engineering, beauty and cosmetics in the field of cancers.

The invention relates to an application of oligonucleotide based on NAT10 gene in preparation of drugs for reversing platinum drug resistance of non-small cell lung cancer. The antisense oligonucleotide provided by the invention not only can reverse platinum drug resistance, but also can inhibit proliferation of non-small cell lung cancer drug-resistant cells, and cell proliferation experiments prove that proliferation of chemotherapy drug-resistant cells is inhibited after treatment; according to the present invention, the tumor cell lipid metabolism abnormality is regulated, the lipid droplet staining results prove that the number of the treated cell lipid droplets is significantly reduced, and the tumor growth can be significantly inhibited, the expression of NAT10 in the tumor tissue can be reduced, the malignant development and metastasis of the tumor can be inhibited, and the anti-tumor effect can be provided in the animal experiment;

The application discloses an oncogene VGLL1 and application of a protein coded by the oncogene VGLL1, and particularly discloses application of a VGLL1 gene and / or a coded protein thereof in preparation of a medicine for treating cancer, and application of the VGLL1 gene and / or the coded protein thereof in preparation of a reagent or a kit for cancer diagnosis and / or prognosis judgment. It is found in the application that the oncogene VGLL1 has an important role in the occurrence and development process of tumors, and high expression of VGLL1 can induce malignant progression such as invasion and metastasis of ovarian cancer. It is also found in the research result that conditionally down-regulating VGLL1 can effectively relieve the growth of ovarian cancer cells and inhibit the invasion and metastasis ability of the ovarian cancer cells. The application provides a new diagnosis and treatment idea and a drug screening platform for solving clinical problems such as metastasis of ovarian cancer.

The invention relates to the technical field of biomedicine, and particularly discloses application of MIDN protein in diagnosis and treatment of glioma. Glioblastoma (GBM) is the most common malignant glioma in the central nervous system and accounts for more than 50% of all glioma, and the existing treatment means face challenges of high drug resistance, poor prognosis and the like. Based on the association between protein degradation imbalance and tumor occurrence and development, the invention finds that MIDN can capture substrate protein through a Catch structural domain thereof and degrade carcinogenic substrate molecules (such as PPDPF) through a non-ubiquitin proteasome pathway, thereby inhibiting the malignant progression of glioma.