67 results about "Nsclc cell" patented technology

The invention provides an alkaloid compound as well as a preparation method and an application thereof in tumor resistance. The alkaloid compound provided by the invention shows a remarkable cytotoxic effect on human non-small cell lung cancer cells A549, mouse lung adenocarcinoma cells Lewis, human triple negative breast cancer cells MDA-MB-231 and mouse breast cancer cells 4T1, and can be used for preparing medicines for treating breast cancer, lung cancer and the like.

The invention discloses an SOD2 knockout cell line and application of the SOD2 knockout cell line in anti-poxvirus, and relates to the technical field of antiviral research. According to the invention, sgRNA of targeted superoxide dismutase 2 (SOD2) is designed, the sequence of the sgRNA is shown as SEQ ID NO.1-SEQ ID NO.2, then a stable SOD2 knockout human-derived non-small cell lung cancer A549 cell line is established by combining CRISPR / Cas9 gene editing with a lentiviral vector delivery technology, single-cell cloning is obtained through multiple rounds of puromycin screening, and the SOD2 gene knockout A549 cell strain is successfully constructed. Vaccinia virus Tian Tan strain infection shows that the number of plaques of SOD2 knockout cells is obviously greater than that of the plaques (about 2.3 times) of normal cell infection, and the plaques are relatively large, so that fine SOD2 has the effect of limiting intercellular transmission of poxvirus. The invention lays a foundation for research and preparation of antiviral drugs.

The invention discloses a polyketone compound derived from actinomycetes as well as a preparation method and application thereof, and relates to the technical field of microbial natural product mining and biological medicine, and the key point of the technical scheme is that the invention discloses a novel polyketone compound Strepactone derived from actinomycetes Streptomyces sp. DP0001, and the molecular formula of the novel polyketone compound Strepactone is C25H38O5. The compound is obtained through strain fermentation, ethyl acetate extraction and multi-step chromatographic purification, and the structure is identified through ESI-MS, 1H NMR and 13C NMR. Experiments show that Strepactone has an inhibition effect on staphylococcus aureus and methicillin-resistant staphylococcus aureus and has remarkable inhibition activity on human non-small cell lung cancer A549 cells, the half inhibitory concentration IC50 of the Strepactone is 5.36 mu M, and the Strepactone has no obvious cytotoxic activity on human embryo kidney cells 293T cells at the concentration of 30 mu M. The compound provided by the invention can be used for preparing anti-drug-resistant bacteria drugs and anti-human non-small cell lung cancer drugs, and also provides a structural basis for the development of novel antibacterial and anti-tumor leading drugs.

The invention discloses a novel pyrimidine KRAS-G12C inhibitor as well as a preparation method and application of the novel pyrimidine KRAS-G12C inhibitor. The pyrimidine compound disclosed by the invention has a remarkable inhibition effect on non-small cell lung cancer cells (NCI-H23 and NCI-H358) with high expression of KRAS-G12C, is particularly used as a medicine for treating and / or preventing the non-small cell lung cancer, is simple and efficient in preparation route, and has a good antitumor medicine development and application prospect.

The present application provides the use of raltitrexed in the manufacture of a medicament for the treatment of diseases caused by adenovirus infection, including but not limited to respiratory tract infection, gastrointestinal infection and keratitis caused by adenovirus. When raltitrexed was tested for its anti-adenovirus activity at the cellular level, using a viral infection dose of 100 TCID50, the viral infectivity was determined on a human non-small cell lung cancer cell line (A549 cell) model, and the results showed that raltitrexed had a significant inhibitory effect on adenovirus, with an EC 50 = 8.98 nM, a CC 50 > 187.5 nM, and it was found that it had a significant inhibitory effect on the entry of the virus into the cell; and in the hDSG2 mouse model, a significant inhibitory effect of raltitrexed on viral replication was also observed. Therefore, raltitrexed can be used to treat diseases caused by adenovirus infection.

The present application relates to the technical field of medicine (IPC classification A61P31 / 22), and particularly relates to a preparation method and application of a tetrahydroindazole antitumor compound, the preparation method comprising: reacting a compound of formula I with adamantanol to obtain a 4-(4-hydrazone-3,6,6-trimethyl-1-tetrahydroindazole)-2-(4-hydroxycyclohexylamino) benzamide compound, compared with a 4-(4-hydrazone-3,6,6-trimethyl-1-tetrahydroindazole)-2-(4-hydroxycyclohexylamino) benzamide compound in the prior art, the compound has stronger inhibition of tumor cell growth activity, has generally lower IC50 values, and in particular can significantly reduce the clonogenicity of non-small cell lung cancer at a low concentration, and causes apoptosis of non-small cell lung cancer cells, and has great significance for development of a novel antitumor drug.

The invention belongs to the field of gene engineering, and particularly designs oligonucleotide and application thereof in preparation of a medicine for treating osimertinib drug-resistant non-small cell lung cancer. Research finds that 3 'tRF-mtAsnGTT is highly expressed in osimertinib drug-resistant non-small cell lung cancer cells, and the inventor designs an effective oligonucleotide capable of specifically inhibiting the function of 3' tRF-mtAsnGTT, so that tumor cell proliferation is inhibited, cell apoptosis is promoted, and the drug sensitivity of the cells to osimertinib is remarkably improved. The invention provides a novel targeting strategy and application approach for molecular intervention and combined treatment of osimertinib resistance of non-small cell lung cancer.

The invention discloses an agonist of a retinoic acid receptor beta and application of the agonist in preparation of a non-small cell lung cancer medicine in the technical field of biological medicine. The agonist of the retinoic acid receptor beta is saturated odd fatty acid heptadecanoic acid C17: 0; according to the research, the expression of a retinoic acid receptor beta can be up-regulated by adding heptadecanoic acid into the NSCLC cells, so that the sensitivity of the NSCLC cells to retinoic acid treatment is improved. When heptadecanoic acid and retinoic acid are combined for use, the activity and migration ability of NSCLC cells can be further inhibited, and apoptosis of the cells is promoted. The result shows that the heptadecanoic acid plays an important role in controlling the sensitivity of the NSCLC cells to the retinoic acid, the combined use of the heptadecanoic acid and the retinoic acid provides a new drug treatment means for treating the NSCLC, and the heptadecanoic acid and the retinoic acid have potential application value in preparing the drug for treating the non-small cell lung cancer.

The invention discloses a nucleotide for inhibiting expression of ILKAP (Interleukin-7-Kinase Associated Protein) related circular RNA (Ribonucleic Acid) and application of the nucleotide, and the nucleotide is characterized in that the nucleotide sequence is CGUCAGUACUCGGGUUUCA, and the expression level of hsacirc0001116 can be specifically and obviously reduced. Experimental results prove that the nucleic acid molecule can effectively interfere with the expression of hsacirc0001116 in human non-small cell lung cancer A549 cells, and can significantly inhibit the survival of lung cancer cells. In addition, when the nucleic acid molecule is combined with an existing antitumor drug for use, a synergistic treatment effect can be generated.

A method for improving the survival of a subject with cancer is disclosed, comprising applying an alternating electric field having a predetermined frequency and electric field intensity to a target site of the subject containing one or more cancer cells for a predetermined period of time, and administering the subject a therapeutically effective amount of a checkpoint inhibitor. A method for treating a subject with cancer is disclosed, comprising applying an alternating electric field having a predetermined frequency and electric field intensity to a target site of the subject containing one or more cancer cells for a predetermined period of time, and administering the subject a therapeutically effective amount of a checkpoint inhibitor. In some embodiments, the checkpoint inhibitor is nivolumab, pembrolizumab, or atezolizumab. Furthermore, a method for improving the survival of a subject with non-small cell lung cancer is disclosed, comprising applying an alternating electric field having a predetermined frequency and electric field intensity to a target site of the subject containing one or more non-small cell lung cancer cells for a predetermined period of time, and administering the subject a therapeutically effective amount of a checkpoint inhibitor. A method for treating a subject having non-small cell lung cancer is disclosed, the method comprising applying an alternating electric field having a predetermined frequency and electric field intensity to a target site of the subject containing one or more non-small cell lung cancer cells for a predetermined period of time, and administering to the subject a therapeutically effective amount of a checkpoint inhibitor. In some embodiments, the checkpoint inhibitor is ipilimumab (Yervoy), pembrolizumab (Keytruda), nivolumab (Opdivo), semiprimab (brand name Ributayo), dostallimab (Jemperli), atezolizumab (Tecentriq), durvalumab (Imfinzi), or avelumab (Bavencio).

The application relates to the technical field of aspirin pharmaceutical chemistry, in particular to an aspirin-sulfonamide hybrid, a preparation method and application thereof. The preparation method can synthesize a plurality of novel aspirin-sulfonamide hybrids by taking piperazine as a bridge, and by a three-step continuous method of "acyl chlorination, sulfonamidation and N-acylation" according to a "molecular hybridization principle". In the process, only one separation and purification is performed, and the preparation steps are simple. The aspirin-sulfonamide hybrid prepared by the method is most effective on human non-small cell lung cancer cells A549, and the activity is more than 33 times higher than that of a parent aspirin, and is similar to the activity of an anticancer drug irinotecan. The aspirin-sulfonamide hybrid 3k prepared by the method has a certain inhibitory effect on various cancer cells. The hybrid can induce human non-small cell lung cancer A549 cell apoptosis in a concentration-dependent manner, and can induce human non-small cell lung cancer A549 cell cycle arrest in the G0 / G1 phase, and inhibit cell growth.

This invention discloses a novel class of β-carboline quaternary ammonium salt derivatives, their preparation methods, and applications. The derivatives have the structure shown in Formula I, where R1, R2, and R3 are various substituents, and X... ‑ It is a halide ion. Its preparation method uses substituted indole-2-methylamine and substituted α-haloacetophenone as starting materials, and constructs them through a one-step cyclization reaction in an aprotic solvent mediated by a catalytic protic acid (such as p-toluenesulfonic acid). This method is mild, simple to operate, requires no metal catalyst, eliminates the risk of metal residue, and has good functional group compatibility. Activity tests of the obtained series of compounds showed that they have significant inhibitory activity against the proliferation of non-small cell lung cancer cell lines (such as A549 and H1299), with some compounds exhibiting activity superior to the positive control drug cisplatin. Therefore, this compound has important application value in the preparation of antitumor drugs, especially anti-lung cancer drugs.

The invention relates to the technical field of biological medicines, in particular to gold nanoparticles modified by arylamine derivatives as well as a preparation method and application of the gold nanoparticles. The gold nanoparticles modified by the arylamine derivatives provided by the invention can improve the endoplasmic reticulum stress level of non-small cell lung cancer cells, can also improve the sensitivity of the non-small cell lung cancer cells to chemotherapeutic drugs, and can improve the death rate of the non-small cell lung cancer cells in cooperation with the chemotherapeutic drugs.

This invention discloses a semi-sandwich structured ruthenium triphenylphosphine dithiocarboxylic acid complex with a simple preparation process and its applications. The complex has the structure shown in Figure (I), with the central ruthenium and... η 5 - Coordination with cyclopentadiene, triphenylphosphine, and dithiocarboxylic acid derivatives, wherein the dithiocarboxylic acid ligands are selected from ethyl xanthic acid, isopropyl xanthic acid, ... N,N Diethyldithiocarbamic acid, morpholine dithiocarbamic acid, and carbazole dithiocarbamic acid. This invention employs a simple one-step method of room temperature preparation and recrystallization purification using a ruthenium precursor and dithiocarbamic acid ligand. This method offers advantages such as readily available raw materials, mild reaction conditions, simple post-processing, and high yield. In vitro tests show that the complexes exhibit excellent anti-proliferative activity against non-small cell lung cancer A549 cells, significantly superior to cisplatin. The complexes demonstrate activity by reducing mitochondrial membrane potential, inducing intracellular reactive oxygen species accumulation, and arresting the cell cycle (G1 phase), leading to late apoptosis in A549 cells.

The application provides an application of PPB in preparation of a drug for preventing or treating non-small cell lung cancer, and relates to the technical field of biological medicines. TRIM47 The CAS number of the PPB is 1415504-32-3. The PPB provided in the application can effectively inhibit the migration and activity of NCI-H1299 cells and SPC-A1 cells, two kinds of non-small cell lung cancer cells, thereby helping to provide a safer and more effective treatment scheme for non-small cell lung cancer treatment.

The application discloses a natural fissistilarin component derivative DhpB and application thereof, and particularly application thereof as a covalent binding ubiquitinase MKRN2 target in anti-KRAS mutant lung cancer. The derivative is from a plant of Peperomia in Piperaceae, can significantly inhibit in-vivo and in-vitro proliferation of KRAS mutant non-small cell lung cancer cells, and induce tumor cell apoptosis through semi-synthetic structure optimization. DhpB is covalently combined with ubiquitinase MKRN2 abnormally expressed in KRAS mutant lung cancer cells, promotes combination of MKRN2 and small ribosomal protein RPS7, thereby promoting ubiquitination and degradation of RPS7, and causes ribosome stress-induced apoptosis of tumor cells. The application provides a new target and inhibitor for preparing a drug for treating refractory KRAS mutant lung cancer, and has a good medicinal prospect.

The invention discloses application of berberine in preparation of a medicine for treating non-small cell lung cancer, and belongs to the technical field of biological medicine. The invention provides an application of berberine in preparation of a medicine for inhibiting or treating EGFR (epidermal growth factor receptor) driven diseases, or an application of berberine combined with other medicines in preparation of a medicine for inhibiting or treating EGFR driven diseases. The diseases comprise non-small cell lung cancer driven by EGFR (epidermal growth factor receptor). It is found that in PC-9 cells, berberine induces ROS accumulation and starts a mitochondrial injury pathway, then mitochondrial membrane potential is reduced, GSDME is activated to form an active N-terminal fragment (GSDME-N), then pyroptosis is induced, NSCLC cell proliferation is inhibited, and berberine is expected to overcome or delay EGFR TKI drug resistance and improve clinical effects and survival prognosis.

The invention relates to the technical field of biomedicine, in particular to a third-generation ALK TKI drug loratinib drug-resistant cell strain as well as a construction method and application thereof, the drug-resistant cell strain is a loratinib-resistant human non-small cell lung cancer cell strain H3122 LS and is preserved in Guangdong Microbial Culture Collection Center on July 25, 2025, and the preservation number is GDMCC No: 66760. According to the invention, an EML4-ALK fusion driven H3122 cell is treated by using a third generation of ALK TKI loratinib, a cell with high drug resistance to loratinib is formed through induction, and it is found that the drug-resistant cell loses EML4-ALK fusion variation. At present, the drug-resistant mechanism of the ALK inhibitor is not clarified clinically, and the construction of the drug-resistant cell and the discovery of the drug-resistant mechanism are beneficial to guiding clinical discovery of a new potential drug-resistant mechanism; a new drug-resistant related driver gene or signal pathway is found, and an experimental basis is provided for subsequent treatment strategy selection of a drug-resistant patient.

This invention relates to the preparation of 10-trifluoromethoxycamptothecin compounds and their use in antitumor drugs. The structural formula of these compounds is shown below. In vitro cytotoxicity screening results show that 10-trifluoromethoxycamptothecin compounds possess broad-spectrum antitumor activity, exhibiting strong inhibitory activity against human hepatocellular carcinoma cells (HepG2), human non-small cell lung cancer cells (A549), human colon cancer cells (SW480), human cholangiocarcinoma cells (QBC939), human breast cancer cells (MCF-7), human pancreatic cancer cells (PANC-1), and human pancreatic cancer cells (BxPC-3). Compounds 10-trifluoromethoxycamptothecin I and 7-ethyl-10-trifluoromethoxycamptothecin II showed strong inhibitory effects against all seven tested tumor cell lines, with IC50 values ​​exceeding 100%. 50 The concentrations were 0.913–0.0661 μM and 4.932–0.0578 μM, respectively, both significantly superior to the control drug topotecan. Among them, compounds I and II exhibited the strongest inhibitory activity against the BxPC-3 cell line, with IC50 values ​​of [missing value]. 50 The values ​​were 0.0661±0.0065μM and 0.0578±0.0043μM, respectively. Therefore, 10-trifluoromethoxycamptothecin compounds hold promise for development into a novel antitumor drug.

The invention discloses preparation and application of a novel magnolol and jatrorrhizine conjugate, relates to the technical field of medicines, and aims to overcome the defects of poor drug resistance and insufficient activity of a single-target anti-cancer drug. According to the technical scheme, acetone or acetonitrile is used as a solvent, and through a two-step substitution reaction, the magnolol and jatrorrhizine conjugate is obtained; the preparation method comprises the following steps: reacting magnolol with dibromo-alkane to generate an intermediate B, and conjugating the intermediate B with jatrorrhizine to obtain a final product with a general formula C; or the jatrorrhizine reacts with dibromo alkane to generate an intermediate E, and then the intermediate E is conjugated with magnolol to obtain the final product of the general formula C. In the preparation process, reaction conditions (such as potassium carbonate alkaline environment and 82 DEG C reflux) are optimized, and high yield and purity are realized. The conjugate disclosed by the invention is widely applied to the anti-tumor field, has remarkable inhibitory activity on various cancer cells (such as non-small cell lung cancer cells HCC827 and human lung adenocarcinoma cells H1975), has better effects than magnolol and jateorhizine monomers, and provides a new candidate for research and development of multi-target drugs.

The invention discloses a short-chain cell-penetrating peptide P3, a targeting drug-loaded micelle and application thereof, the sequence of the short-chain cell-penetrating peptide P3 is Trp-Lys-Ala-Ser-Cys (WKASC), and the peptide sequence containing the function covers all derivative peptide sequences which take the five peptide sequences as a skeleton and are connected with other functional amino acids or short peptide sequences at the N end or the C end. The invention can realize efficient recognition and penetration of in vivo / in vitro non-small cell lung cancer cells, and has the characteristics of low cytotoxicity, good biocompatibility, no significant hemolytic toxicity and the like. A targeting delivery system can be constructed by coupling the polymer carrier with a polymer carrier and loading a chemotherapeutic drug (such as adriamycin). The system can effectively overcome biological barriers, improve enrichment of drugs in tumor tissues and intracellular delivery efficiency, significantly inhibit tumor growth, reduce systemic toxicity and side effects, and provide a new strategy for precise treatment of lung cancer.

The invention belongs to the technical field of polypeptide drugs, and particularly relates to a series of polypeptides with an anti-cancer effect and application thereof. According to the invention, Rink amide MBHA amino resin is used as a solid phase carrier, modification is carried out according to an amino acid sequence of a template polypeptide Hymenochirin-1Pa (H-0): Ac-LKLSPKTKDTLKKVLKGAIKGAIAIASAMA-NH2, and on the basis of retaining key amino acid residues, original amino acids are replaced by R8 and S5 at the positions of i and i + 7 amino acids, so that the target stapling peptide is obtained. Compared with a template polypeptide H-0, the obtained stapled peptide has the advantage that the anti-tumor activity on human liver cancer cells Huh7, human non-small cell lung cancer cells A549, glioma cells U87 and colon cancer cells T84 can be obviously improved.

The invention belongs to the field of biological pharmacy, and discloses a chalcanthicidin compound and application thereof in preparation of antitumor drugs. The chalcanthicidin compound is separated from a secondary metabolite of marine actinomycetes Streptomyces sp. KCB-132, and the chalcanthicidin compound is named as Gricidin A. The chalcanthicidin compound has the advantages that the chalcanthicidin compound can be used for preparing the chalcanthicidin compound; an anti-tumor activity experiment discovers that the Gricidin A has a remarkable inhibition effect on three strains of non-small cell lung cancer cells (NCI-H460, NCI-H1975 and A549), and has the potential of being developed into the medicine for treating the non-small cell lung cancer.

The invention belongs to the field of biotechnology and medicine, provides application of thioredoxin TXN1 and TRP14 as a bidirectional switch for regulating and controlling a cell death mode and application of an anti-cancer drug, and particularly relates to new application of TXN1 and TRP14. The invention reveals that TXN1 and TRP14 play a role of a bidirectional regulation switch in regulating the sensitivity of non-small cell lung cancer cells to different programmed death modes (including apoptosis, ferroptosis and disulfide death) for the first time. By reducing the activity or expression of TXN1 or TRP14, the sensitivity of cancer cells to apoptosis inducers and ferroptosis inducers can be enhanced, but the resistance of the cancer cells to glucose deprivation-induced disulfide death is remarkably enhanced. The discovery shows that inhibition of TXN1 / TRP14 can be combined with an apoptosis / ferroptosis inducer to treat cancers; meanwhile, an inhibitor aiming at TXN1 / TRP14 can be used for preventing or treating diseases related to disulfide death. The invention provides a cancer treatment composition based on the discovery, a drug screening method and biomarker application.

Disclosed is a method of increasing lifetime of a subject having cancer, the method comprising: applying an alternating electric field to a target site of the subject for a period of time, the alternating electric field having a frequency and a field strength, where the target site comprises one or more cancer cells; and administering to the subject a therapeutically effective amount of a checkpoint inhibitor. Disclosed is a method of treating a subject having cancer, the method comprising: applying an alternating electric field to a target site of the subject for a period of time, the alternating electric field having a frequency and a field strength, where the target site comprises one or more cancer cells; and administering to the subject a therapeutically effective amount of a checkpoint inhibitor. In some aspects, the checkpoint inhibitor is Nasuliumab, palbolizumab, or atelizumab. Also disclosed is a method of increasing the lifetime of a subject suffering from non-small cell lung cancer, the method comprising: applying an alternating electric field to a target site of the subject for a period of time, the alternating electric field having a frequency and a field strength, where the target site comprises one or more non-small cell lung cancer cells; and administering to the subject a therapeutically effective amount of a checkpoint inhibitor. Disclosed is a method of treating a subject suffering from non-small cell lung cancer, the method comprising: applying an alternating electric field to a target site of the subject for a period of time, the alternating electric field having a frequency and a field strength, where the target site comprises one or more non-small cell lung cancer cells; and administering to the subject a therapeutically effective amount of a checkpoint inhibitor. In some aspects, the immune checkpoint inhibitor is an irpimumab (Yvoy), a palborizumab (Keytruda), a Nasuliumab (Opdivo), a samipril monoclonal antibody (trade name Libtayo), as well as a doemperli monoclonal antibody (Jemperli), an artirizumab (Tecentriq), a duvalriumab (Imfinzi), or an averticib (Bavencio).

This invention relates to the pharmaceutical applications of MRPS7 as a diagnostic biomarker for non-small cell lung cancer (NSCLC) and its inhibitors, belonging to the field of biomedical technology. For the first time, this invention utilizes immunohistochemical analysis of tumor tissues from NSCLC patients and paired adjacent normal tissues to confirm that MRPS7 protein is significantly overexpressed in NSCLC tissues (p<0.001), and this difference is statistically significant in both lung adenocarcinoma and lung squamous cell carcinoma subtypes. Furthermore, this invention demonstrates through in vitro functional experiments that knocking down MRPS7 gene expression using siRNA targeting MRPS7 significantly inhibits the proliferation, migration, and invasion abilities of NSCLC cells (A549, SK-MES-1) (p<0.001). Therefore, reagents for detecting MRPS7 expression levels can be used to prepare NSCLC diagnostic products, and MRPS7 inhibitors can be used to prepare drugs for treating NSCLC. This invention provides a novel molecular biomarker for the diagnosis of NSCLC and a new strategy for targeted therapy of NSCLC.

This invention relates to the field of biomedical technology, providing the application of ACAT1 in the preparation of diagnostic and prognostic products for non-small cell lung cancer (NSCLC). Compared to existing technologies, the ACAT1 expressed in this invention is decreased in tumor tissues, and this decreased ACAT1 expression is associated with overall survival (OS) and progression-free survival (PFS), indicating a poor prognosis. Therefore, ACAT1 can serve as a biomarker for the diagnosis and prognostic prediction of NSCLC, inhibiting NSCLC cell proliferation and migration. Furthermore, as a key enzyme in β-oxidation, ACAT1 promotes fatty acid oxidation, thereby reducing intracellular lipid accumulation, and has the potential to inhibit disease progression by regulating lipid metabolism in NSCLC.

The application discloses a kind of targeted nanomedicine for treating radiation-resistant NSCLC and its preparation method and application, and belongs to the medical technical field, wherein the preparation method of targeted nanomedicine includes the following steps: using NaGdF4 as core, mesoporous silica as carrier, NaGdF4 is coated, and radio-sensitizing nanomaterial is obtained;Radio-sensitizing nanomaterial is co-incubated with PD-1 protein, and the targeted nanomedicine for treating radiation-resistant NSCLC is obtained.The application regulates radiation-resistant NSCLC tumor immune microenvironment by constructing radiosensitizing nano platform and loading PD-1 protein, controls the proliferation, migration and invasion of radiation-resistant NSCLC cells, successfully reverses the radioresistance of NSCLC, and significantly enhances the response of resistant cells to radiotherapy.The method provides valuable insights for developing targeted nanotherapeutic drugs to effectively treat NSCLC.

The invention discloses an application of melanine in preparation of an antitumor drug. The invention proposes and verifies that the melanine can significantly inhibit the cell proliferation activity of the epidermal growth factor receptor mutant non-small cell lung cancer by inducing ferroptosis for the first time, and significantly inhibit the migration and diffusion of cancer cells and the colony proliferation and tumorigenesis potential of the cancer cells; and a new choice and direction are provided for clinical treatment of the epidermal growth factor receptor mutant non-small cell lung cancer.

The present invention belongs to the field of biomedical technology, and specifically relates to a new application for piR-hsa-164586 and MYH9, based on the interaction between piR-hsa-164586 and MYH9: piR-hsa-164586 regulates the expression of MYH9 and promotes the metastasis of NSCLC, piR-hsa-164586 and MYH9 can be used as a therapeutic target for NSCLC, and have become a potential therapeutic drug, wherein the MYH9 is obtained by RNA pulldown assay and verified by protein mass spectrometry, molecular docking and RIP assays, the piR-hsa-164586 can positively regulate the expression of MYH9, and verified by performed qRT-PCR, western blotting and tissue immunofluorescence staining assays on the piR-hsa-164586 NC group, piR-hsa-164586 KD group, and piR-hsa-164586 OE group. The interaction between piR-hsa-164586 and MYH9 can up-regulate the expression of MYH9 in NSCLC cell lines, the verification experiment process was confirmed by Transwell experiment after knockdown of piR-hsa-164586 and MYH9 respectively.