52 results about "Tumor suppressor gene" patented technology

The invention provides application of a PDLIM4 gene in preparation of a medicine for inhibiting non-small cell lung cancer proliferation, belongs to the technical field of cancer suppressor gene research, and finds that the PDLIM4 gene is highly expressed in non-small cell lung cancer tumors, and the prognosis of a patient with the highly expressed PDLIM4 gene is good; the proliferation of the non-small cell lung cancer cells overexpressed with the PDLIM4 gene is inhibited, and the proliferation of the non-small cell lung cancer cells knocked down with the PDLIM4 gene is accelerated, so that the reagent capable of realizing the overexpression of the PDLIM4 gene is confirmed to be of great significance for inhibiting the proliferation of the non-small cell lung cancer cells. The overexpression of the PDLIM4 gene in the non-small cell lung cancer cells can enhance the chemotherapy effect of the chemotherapy drug adriamycin, and can be used as a chemotherapy sensitizer. The BRD4 is an upstream regulatory factor for increasing the expression of the PDLIM4 gene in the non-small cell lung cancer, and can be used for promoting the expression of the PDLIM4 gene.

The invention relates to a method for forming a hair follicle-like structure by co-culturing an immortalized hair papilla cell line derived from human hair follicles and keratinocytes. Specifically disclosed is a hair papilla cell line (SV40T-hTERT DPC) which is immortalized by forced expression of SV40T, which deactivates a cancer suppressor gene, in human hair follicle-derived hair papilla cells and hTERT gene, which is a telomerase elongase promoting gene, and keratinocytes, are co-cultured three-dimensionally. From the result, it has been confirmed that a hair follicle-like structure is formed in which a cuticle grows so that a hair follicle analogue in combination with a primary-cuticle hair follicle-derived cell has a shape similar to that of the primary-cuticle hair follicle-derived cell. Therefore, the method can be applied to multiple fields of animal replacement experiments, efficacy evaluation of materials for preventing alopecia / promoting hair follicle growth and the like. Through immortalized hair papilla cells, higher result consistency can be ensured compared with that in the prior art, and stable hair follicle-derived cell supply can be realized, so that the problem of high entry barriers of efficacy evaluation of alopecia materials based on cells is expected to be solved.

The invention discloses a compound for specific targeted degradation of PIN1 protein and application, and belongs to the technical field of biological medicine, the structural general formula of the compound is as shown in formula I # imgabs0 #, X is any one of-CH2-,-NH-and-O-; linker is any structure of C3-12 alkyl, C3-12 alkoxy and a formula II, n represents any number between 1 and 4, A represents-N-or-CH-, and Cy represents an aromatic ring, an aromatic heterocyclic ring or a saturated carbocyclic ring with the carbon number of 3-6; the # imgabs1 # E3L is any one structure in a formula III; according to the present invention, the PIN1 protein can be subjected to targeted degradation in a variety of tumor cells so as to reduce the PIN1-mediated cancer promoting gene expression while up-regulating the PIN1-inhibited cancer suppressor gene.

The invention belongs to the technical field of biological medicine and molecular biology, and provides application of GJB6 in preparation of an esophageal squamous cell carcinoma prognosis evaluation reagent and screening of drugs for targeted treatment of esophageal squamous cell carcinoma. The low expression of the GJB6 is applied to preparation of an esophageal squamous cell carcinoma prognosis evaluation reagent. GJB6 is low in expression in ESCC patients, and ESCC prognosis is poor. And the prognosis of patients with high expression of GJB6 is better. Overexpression of GJB6 inhibits ESCC cell proliferation, migration and invasion and in-vivo tumor enlargement. The GJB6 plays a role of a cancer suppressor gene in ESCC and inhibits cell proliferation, migration and invasion. The AKT signal channel is one of downstream channels for GJB6 to regulate the occurrence and development of ESCC. The AKT inhibitor effectively inhibits GJB6 low-expression ESCC malignant phenotypes, including enhancement of cell proliferation and migration invasion ability and in-vivo tumor enlargement. The AKT is a key therapeutic target of the GJB6 low expression type ESCC.

The invention discloses an oncolytic virus and application of the oncolytic virus in preparation of tumor inhibition drugs. The oncolytic virus is a lentiviral vector, and the lentiviral vector comprises polynucleotide encoding p16 protein or a bioactive part of the p16 protein containing CDKN2A gene, and can effectively inhibit growth of cancer related to CDKN2A gene mutation, so that the problem that the existing oncolytic virus has biological safety risk in delivery of cancer suppressor genes is effectively solved.

Provided herein are methods and compositions for treating cancer in an individual comprising administering to the individual an effective amount of at least one CD122 / CD132 agonist, at least one immune checkpoint inhibitor and a viral composition comprising one or more viruses engineered to overexpress a tumor suppressor gene and / or an adenoviral death protein. Also provided herein are methods and compositions for treating cancer in an individual comprising administering to the individual an effective amount of at least one oncolytic viral composition and at least one CD122 / CD132 agonist and at least one immune checkpoint inhibitor. Also provided herein are methods of enhancing anti-tumor efficacy by administering the agents described above in combination with other cancer therapies. In highly aggressive forms of cancer, known to be generally resistant to immune therapies, these treatments unexpectedly resulted in complete tumor remissions and curative outcomes.

The invention discloses an elephant source bacillus licheniformis and application thereof. The preservation number of the bacillus licheniformis strain L517 is GDMCC 67825, the bacillus licheniformis strain L517 is classified and named as bacillus licheniformis, and the preservation date is February 26, 2026. Research finds that the bacillus licheniformis has a remarkable treatment effect on acute colitis of mice; and the traditional Chinese medicine composition also has a remarkable treatment effect on mouse subcutaneous colon cancer. The anti-cancer mechanism is that the infiltration of GZMB < + > CD8 < + > cytotoxic T cells in a tumor microenvironment is remarkably promoted in vivo through a supernatant metabolite of a culture medium, and a tumor suppressor gene P53 can be directly up-regulated. It is found for the first time that the elephant intestinal tract source bacillus licheniformis with evolutionary disease-resistant advantages shows good anti-proctitis and colon cancer activity, and can become an effective medicine for treating proctitis and colon cancer in the future.

The invention discloses an immortalized rabbit liver cell line as well as a construction method and application thereof, and the construction method is characterized in that an exogenous oTERT gene is introduced into rabbit embryo liver cells, so that the rabbit embryo liver cell line is immortalized. The successfully immortalized rabbit embryo liver cell line can be stably subcultured for more than 10 generations, and does not have an aging phenomenon. Compared with a traditional method (introducing exogenous immortalized genes such as cancer suppressor genes p53 and SV40TAg into cells), the TERT-mediated cells belong to normal cells, the growth characteristics of the TERT-mediated cells are kept consistent with those of the normal cells, the TERT-mediated cells belong to immortalization in a real sense, and a scientific and stable cell material can be provided for subsequent RHDV research. The construction method is simple, easy to implement and easy to popularize.

The invention belongs to the technical field of biological medicines, and particularly relates to application of a cancer suppressor gene SLC26A11 in hyperleukocyte acute B lymphocytic leukemia. The invention discloses an application of a cancer suppressor gene SLC26A11 as a specific molecular marker in preparation of induction treatment reaction, prognosis and risk assessment of high leukocyte acute B lymphocytic leukemia of children, and an application in improvement of sensitivity of chemotherapeutic drugs for high leukocyte acute B lymphocytic leukemia of children. The SLC26A11 is used as a potential target, so that a personalized treatment scheme is provided for HALL patients, the toxic and side effects of chemotherapeutic drugs are reduced, and the treatment effect is improved.

Disclosed herein is a system that addresses all of the current challenges described above by combining three existing technologies and an improved nuclear RNA delivery system to generate a first-in-class cellular therapy that can secrete a cancer specific suicide gene for the treatment of several cancers. Also disclosed herein is a 'Trojan-Horse' like genetic construct aimed at engineering a chemo-sensitive dominant clone for adaptive therapy in cancers, such as leukemia. In some embodiments, cells, such as cancer cells from a subject, are engineered with suicide genes to promote a bystander effect in neighboring cancer cells once returned to the subject. In some embodiments, these cells are further engineered to be clonally dominant, e.g. by deleting or mutating tumor suppressor genes in the cells, overexpressing oncogenes, or any combination thereof. Once the engineered cells have reached a target clonal dominance, the suicide gene can be induced, thereby promoting the bystander effect.

Mutations of oncogenes and tumor suppressor genes promote the development and progression of cancer. The present disclosure describes compounds and methods for restoring wild type function of p53 mutants. The compounds of the present invention can bind to mutant p53 and restore the ability of the p53 mutant to bind to DNA and activate downstream effectors involved in tumor suppression. The disclosed compounds can be used to reduce the progression of cancers containing p53 mutations.

Methods for inducing basal cell carcinoma (BCC) or BCC tumors, as well as an inducible non-human animal models of BCC, are defined herein. The methods and animal models comprise targeting Ptch1 and / or a tumor suppressor gene via conditional expression of one or more short hairpin RNAs (shRNAs) in the skin of said animals.

Provided are a method and a combination for one-tube simultaneous detection of tumor-specific gene mutation and methylation, and the use thereof. The method comprises searching a database to select mutation and methylation sites of a cancer driver gene and a cancer suppressor gene, synthesizing capture probes correspondingly paired with a target interval, performing hybrid capture on an amplification product of a sample treated with a restriction endonuclease by using a probe set comprising tumor-specific gene mutation and methylation capture probes, constructing a high-throughput sequencing library containing a target region, and performing high-throughput sequencing to obtain the sequence of a target fragment, so as to obtain the results of methylation, point mutations and indel variation of a cancer-associated gene. The provided method enables one-tube simultaneous detection of mutation and methylation states of a cancer-associated gene in one assay, requires a low content of a gene to be detected, can be used for methylation and mutation detection of a tumor-specific DNA, and has low detection costs and high efficiency.

Provided are a multi-gene nanocarrier, a preparation method therefor, an application thereof, and an anti-cancer drug. The multi-gene nanocarrier comprises a three-branch central ligand and gene combination sequences covalently connected on each branch of the three-branch central ligand, the gene combination sequences on each branch all being the same; in the direction from the three-branch central ligand outward, the gene combination sequences contain at least two tumor suppressor genes selected in order from among TP53, BIM, and PTEN. The provided multi-gene nanocarrier has excellent anti-cancer activity and biological safety.

Application of TMOD3 and / or ADSL in non-small cell carcinoma. The present invention discloses the application of reagents for detecting the expression levels of TMOD3 and / or ADSL in the preparation of products for detecting non-small cell lung cancer. The present invention also discloses the application of an ADSL promoter in the preparation of a drug for treating non-small cell lung cancer. The present invention reveals that the new NSCLC oncogene TMOD3 and tumor suppressor gene ADSL play important roles in the malignant progression and ferroptosis of non-small cell lung cancer and their potential molecular mechanisms, which can provide a basis for the diagnosis, treatment and prognosis of NSCLC, and provide a new research direction and theoretical basis for precision treatment.

The invention provides application of ITIH2 in treatment of gastric cancer. According to the invention, a Mendel randomization (MR) method in a drug genome range is utilized, and it is determined that ITIH2 is a potential drug target of gastric cancer. In-vitro studies show that ITIH2, as a tumor suppressor gene, significantly inhibits growth and migration of gastric cancer cells. After standard screening, a drug approved by FDA, namely amiodarone, is preferentially considered, the amiodarone serves as a reutilization drug for treating the gastric cancer, and the effectiveness of the amiodarone is verified by inhibiting growth and migration of gastric cancer cells and angiogenesis. In a word, the research provides a new insight for gene-based gastric cancer drug treatment, and potential possibility is provided for success of clinical experiments.

The present invention belongs to the field of gene therapy or biological gene technology, and particularly relates to a gene combination and its expression vector and use. The gene combination is used to exist and express in nasal cells; including: U6 promoter and downstream sgRNA gene and tandem tumor suppressor gene, wherein the sgRNA gene targets tumor suppressor gene; super hTERT promoter and downstream dCas9 gene and / or miniSaCas9 gene, and tandem VP64 gene; SPLUNC1 promoter and downstream artificial miRNA gene; wherein, U6 promoter, super hTERT promoter, dCas9 gene, miniSaCas9 gene, VP64 gene, SPLUNC1 promoter and artificial miRNA gene are shown in SEQ ID NO.1-7 in sequence. The sgRNA initiated by U6 promoter and the dCas9-VP64 initiated by super hTERT are tandemly activated to activate downstream tumor suppressor genes, such as P53, etc., and finally cause apoptosis of nasopharyngeal carcinoma cells, thereby achieving treatment of nasopharyngeal carcinoma.

Mutations in oncogenes and tumor suppressors contribute to the development and progression of cancer. Disclosed herein are compounds and methods to recover wild-type function of p53 mutants using x-ray co-crystal structures of mutant p53 and compounds of the disclosure. The compounds of the present invention can bind to mutant p53 and restore the ability of the p53 mutant to bind DNA and activate downstream effectors involved in tumor suppression. The disclosed compounds can be used to reduce the progression of cancers that contain a p53 mutation.

The invention discloses an anti-BCL6 protein nano antibody, a fusion protein and application thereof, and belongs to the technical field of biology. According to the invention, the nano antibody specifically targeting BCL6 is designed by using an artificial intelligence technology, and the nano antibody has good specificity and high affinity, and can efficiently bind to a BCL6 antigen; furthermore, rational design of the nano-antibody is carried out through artificial intelligence, so that a nano-antibody mutant with higher affinity is obtained; furthermore, a nano antibody or a nano antibody mutant with high affinity and relatively good specificity is fused with an RBCC structural domain or a mutant thereof to obtain a fusion protein, and the fusion protein can utilize the specificity of the nano antibody structural domain to bind to a target protein and start a protein degradation pathway, so that targeted degradation of the BCL6 protein is realized, and the BCL6 protein can be degraded in a targeted manner. The expression of cancer suppressor genes p53 and cyclin p21 in cells is improved, and the method has a very great clinical application value.

To provide application of a tumor suppressor gene.SOLUTION: Two antibodies capable of binding to a mutated P53 protein are created to sandwich the P53 protein from both sides for detection. The entire molecule thus sandwiched constitutes a transcription factor. The transcription factor expresses a toxin.

Mutations in oncogenes and tumor suppressors contribute to the development and progression of cancer. The present disclosure describes compounds and methods to recover wild-type function to p53 mutants. The compounds of the present invention can bind to mutant p53 and restore the ability of the p53 mutant to bind DNA and activate downstream effectors involved in tumor suppression. The disclosed compounds can be used to reduce the progression of cancers that contain a p53 mutation.

The present disclosure relates to methods of treating pancreatic cancer. In particular, methods of treating pancreatic cancer and limiting overexpression of oncogenes, activating tumor suppressor genes, or modulating signaling proteins in a patient are described, comprising administering a compound and a pharmaceutical combination as described herein.

The invention discloses an application of an epigenetic drug combined with adoptive monocyte / macrophage immunotherapy in the preparation of a biopharmaceutical for tumor diseases, belonging to the technical field of biopharmaceuticals. The present invention provides an application of an epigenetic drug combined with adoptive monocyte / macrophage immunotherapy in the preparation of a biopharmaceutical for tumor diseases, wherein the epigenetic drug removes the methylation of tumor cells, increases the susceptibility of tumors to targeted therapy and regulates tumor heterogeneity, and the chimeric antigen receptor extracellular domain of the CAR monocyte / macrophage targets and recognizes and blocks the signal pathway of targeted tumor antigens, and performs cellular immune killing. The epigenetic modification of the present invention and CAR monocyte / macrophage anti-solid tumor treatment have a synergistic therapeutic effect, and the epigenetic modification treatment makes tumor antigens more sensitive to CAR monocyte / macrophage therapy, promotes the expression of tumor suppressor genes, promotes the conversion of tumor cell apoptosis to pyroptosis, and solves the problem of immune escape tolerance caused by tumor heterogeneity.

This invention relates to the engineering of animal cells, preferably mammalian, more preferably rat, that are deficient due to the disruption of tumor suppressor gene(s) or gene product(s). In another aspect, the invention relates to genetically modified rats, as well as the descendants and ancestors of such animals, which are animal models of human cancer and methods of their use.

The invention discloses an octopus-shaped CdS QDs net and multivalent Au-S bond mediated photoelectrochemical detection strategy method for TP53. The method comprises the following steps: (1) preparing a TiO2-MXene (at) Au photoelectrode; (2) carrying out target identification and signal amplification reaction; and (3) adding a reaction solution obtained in the step (2) to the TiO2-MXene (at) Au photoelectrode obtained in the step (1) as a working electrode, and carrying out PEC measurement by taking a platinum wire as a counter electrode. An octopus-shaped CdS QDs net is formed based on a terminal deoxynucleotidyl transferase (TdT) chain extension reaction and a biotin-streptavidin coupling reaction, and a large number of CdS QDs can be enriched to the surface of the electrode through multivalent Au-S bond anchoring, so that the output of photoelectric signals is enhanced, and the sensitive detection of the cancer suppressor gene TP53 is realized.

The present invention discloses a non-invasive early screening method and system for cancer based on the length distribution characteristics of cfDNA fragments. This method uses a relatively low-depth whole-genome sequencing method to statistically analyze the differences in the fragment length distribution characteristics of tumor-derived cfDNA and healthy individual-derived cfDNA, establish an early screening model for cancer, and achieve non-invasive early screening for cancer. The scheme of the present invention focuses on the characteristic of blood cfDNA fragment size to distinguish ctDNA from non-tumor-derived cfDNA. It does not rely on the mutation detection of oncogenes or tumor suppressor genes, and eliminates the interference caused by clonal hematopoietic mutations. Secondly, the data of the embodiments of the present invention show that the size characteristics of blood cfDNA fragments can be used to distinguish between healthy people and early-stage tumor patients. Finally, due to the use of low-depth whole-genome sequencing technology, the detection costs involved in the scheme of the present invention are greatly reduced, which is conducive to future applications in the field of early screening of malignant tumors.

The present invention relates to a use of untranslated RNA RP11-252E2.2 for predicting liver cancer metastasis or treating liver cancer metastasis. lncRNA which specifically decrease in expression in liver cancer tissues and cells were identified by analyzing lncRNA which specifically decrease in expression in liver cancer as compared to normal cells with respect to lncRNA showing the potential to function as tumor suppressor genes, and RP11-252E2.2 was found to be involved in the metastasis of liver cancer. Therefore, the untranslated RNA RP11-252E2.2 discovered in the present invention is highly likely to be effectively used for predicting or treating liver cancer metastasis.

The present invention belongs to the field of biotechnology, and specifically relates to a biomarker for breast cancer, the ZNF662 gene, and its detection method and application. The biomarker is the ZNF662 gene, and the sample to be tested is derived from a patient suspected of breast cancer. The nucleotide of the ZNF662 gene is SEQ ID NO: 1. The present application provides a method for detecting the methylation status of the ZNF662 gene promoter, and the specific steps are: ① extracting a DNA sample; ② designing primers, using a methylation detection reagent, and detecting the methylation level of the ZNF662 gene promoter in the DNA sample by the MSP method to determine whether the ZNF662 gene is methylated, thereby achieving breast cancer diagnosis. The present application is the first to confirm through in vivo and in vitro experiments that ZNF662 is a new tumor suppressor gene, and its expression is downregulated in breast cancer due to hypermethylation of the promoter, providing a new option for the screening of early diagnostic markers for breast cancer.

A tumor microenvironment regulation composite gene vector and its preparation method and application belong to the technical field of biomedical organic polymer materials. In order to solve the technical problems of low transfection efficiency and target cell selectivity of non-viral gene vectors in the prior art, the present invention provides a tumor microenvironment regulation composite gene vector, the composite gene vector includes the following components: macrophage polarizer BLZ945, silk fibroin, polyethyleneimine and pDNA expressing tumor suppressor gene; the packaging form of the composite gene vector is mixed packaging or layer packaging. The composite gene vector provided by the present invention has the function of converting the tumor-promoting phenotype of tumor-associated macrophages into an anti-tumor phenotype, reshaping the immunosuppressive tumor microenvironment, regulating the tumor microenvironment, and improving the immune anti-tumor effect; the composite gene vector can transfer anti-tumor genes into tumor cells, inhibit the proliferation and apoptosis of tumor cells, and can be used to prepare anti-tumor drugs.

Provided are a corn peptide having an anti-tumor effect, and a preparation method therefor and a use thereof. The corn peptide can obviously eliminate reactive oxygen species in tumor cells, increase the concentration of free calcium ions in the cytoplasm of the tumor cells and reduce the mitochondrial membrane potential of the tumor cells, and also can enhance the expression levels of mRNA and proteins of an IP3R and calreticulin, and further affect the calcium homeostasis of the tumor cells. In addition, the corn peptide can up-regulate the expression of tumor suppressor genes PTEN, P21 and P27, down-regulate the expression of a cell proliferation marker PCNA and a tumor-promoting gene Akt, and mediate an anti-tumor effect by means of PTEN and Akt cell signaling pathways.