70results about How to "Increased chemosensitivity" patented technology

The present invention provides novel anticode oligomers and methods of using them for controlling the growth of cancer cells expressing the bcl-2 gene.

It has now been determined that antisense therapy which reduces the expression of TRPM-2 provides therapeutic benefits in the treatment of cancer. In particular, such antisense therapy can be applied in treatment of prostate cancer and renal cell cancer. Addition of antisense TRPM-2 ODN to prostatic tumor cells in vivo is effective for delaying the onset of androgen independence. Thus, prostate cancer can be treated in an individual suffering from prostate cancer by initiating androgen-withdrawal to induce apoptotic cell death of prostatic tumor cells in the individual, and administering to the individual a composition effective to inhibit expression of TRPM-2 by the tumor cells, thereby delaying the progression of prostatic tumor cells to an androgen-independent state in an individual Combined use of antisense TRPM-2 and taxanes synergistically enhances cytotoxic chemosensitivity of androgen-independent prostate cancer. In addition, it has also been found that antisense TRPM-2 has beneficial effect for other cancer types. Specifically, antisense TRPM-2 ODN enhances chemosensitivity in human Renal cell cancer, a normally chemoresistant disease with no active chemotherapeutic agent having an objective response rate higher than 10%. Radiation sensitivity is also enhanced when cells expressing TRPM-2 are treated with antisense TRPM-2 ODN. Thus, the antisense TRPM-2 ODNs can be used to enhance hormone sensitivity, chemosensitivity and radiation sensitivity of a variety of cancer types in which expression of TRPM-2 has been observed.

The invention relates to a method for establishing a paclitaxel (PTX)-resistant ovarian cancer cell model. The method comprises the following specific steps: intervening an OVCAR-3 cell and an SK-OV-3 cell by virtue of PTX, replacing a PTX-free culture medium, intervening the OVCAR-3 cell and the SK-OV-3 cell until growth of cells returns to be normal, namely, under the conditions that the cells stably grow, morphologies are full, no floating dead cells are produced and the passage density is 30%, enabling the cells to grow 90% in 3-5 days, starting to carry out normal passage and improving the concentration of PTX, wherein the intervention time for each time is 24 hours; and finally obtaining the PTX-resistant ovarian cancer cell model having the preservation numbers of CCTCC C2014203 and CCTCC C2014204. According to the method, by closely observing growth states of cells and selecting the intervention moment, the established cell model has higher level of drug-resistance coefficients and good resistance stability and can be used for the research on ovarian cancer drug-resistant mechanism, ovarian cancer drug-resistant reversion, prevention of chemotherapy resistance and the improvement on chemosensitivity.

The invention provides novel inhibitors of protein translation initiation and inhibitors of eIF4F activity that can increase chemosensitivity or diminish or reverse chemoresistance in growth transformed cells and thereby reduce hyperproliferative conditions, such as cancer progression, in select patient populations having particular tumor genotypes. The invention also provides methods which target translation initiation controls in growth-transformed cells, such as tumor subtypes with altered expression of a gene activity, including the human akt, bcl-2, eIF4E, eIF4A or PTEN activities, to restore drug sensitivity in vivo in a genotype selective manner. In one aspect, the inhibitors of translation initiation of the invention are rocaglates, i.e., cyclopenta[b]benzofurons, which increases chemosensitivity or diminishes or reverses chemoresistance either alone or in combination, additively or synergistically, with other agents that alter growth or death. Preferably, the rocaglate is silvestrol, which is used alone or in combination with doxorubicin to reverses chemoresistance in PTEN-deficient lymphomas or eIF4E-over-expressing lymphomas and to promote cancer remission.

The invention provides novel prodrugs of inhibitors of PI-3 kinase. The novel compounds are LY294002 and analogs thereof comprising a reversibly quaternized amine.

The present invention relates to a marker piRNA-54265 and a method in diagnosis, treatment, and prognostic evaluation of colorectal cancer. The marker piRNA-54265 is capable of being used for diagnosing and/or treating colorectal cancer, wherein the marker piRNA-54265 is selected from any of molecules as follows: (1) SEQ ID NO.29: tggaggtgatgaactgtctgagcctgacc; (2) SEQ ID NO.30: UGGAGGUGAUGAACUGUCUGAGCCUGACC; (3) SEQ ID NO.31: GGUCAGGCUCAGACAGUUCAUCACCUCCA; (4) a piR-54265 variant and a piR-54265 derivative modified from the molecule shown in (1), (2) or (3) with a same function; (5) a piR-54265 polynucleotide construct capable of down-regulating an amount of the piR-54265 in vivo after being introduced; and (6) an expression vector containing the polynucleotide construct of (5). The method is used for diagnosing/screening colorectal cancer, evaluating chemosensitivity of a colorectal cancer patient, evaluating a prognosis of a colorectal cancer patient or treating colorectal cancer.

The invention relates to methods of diagnosis and prognosis of cancer, and in particular NSCLC, the methods comprising determining the expression level of one or more genes. In some embodiments the invention relates to prognosis of early stage NSCLC.

The invention belongs to the technical field of biology, particularly relates to the field of medical diagnosis, in particular to application of TRERNA1 gene to prediction and improvement of sensitivity of liver cancer drug sorafenib. The prognosis of hepatocellular carcinoma and the evaluation of chemotherapy resistance of liver cancer are marked, and the expression level of TRERNA1 genes is detected by utilizing an RNA in-situ hybridization technology or qPCR, so that the prognosis and chemotherapy resistance of the hepatocellular carcinoma can be obtained, the introduction way of the TRERNA1 is simple, the whole prediction and evaluation process is simple and easy, and the feasibility is high.

The invention discloses application of ATF3 as a target site in preparing a taxol chemosensitization medicine for treating nasopharynx cancer. Tests show that the expression level of an Activating transfactor 3 ATF3 in nasopharynx cancer taxol drug-resistant cells is remarkably lower than that of taxol sensitive cells, and in addition, ATF3 is capable of improving the taxol chemosensitization of nasopharynx cancer by regulating and controlling HIPPO signal paths. Therefore, ATF3 can be used as a potential target site for chemosensitization treatment on nasopharynx cancer. As the target site, ATF3 can be used for preparing nasopharynx cancer chemosensitization treatment medicines, and particularly as the target site, ATF3 can be used for preparing medicines for regulating and controlling HIPPO paths to improve taxol chemosensitization of nasopharyngeal carcinoma cells.

The invention relates to the field of medicines, and discloses novel application of gossypol. The gossypol can be used for effectively inhibiting the activity of NF-kappa B, AP-1 and HIF-1 alpha which are induced by reduction-oxidation of APE1 (apurinic/apyrimidinic endonuclease-1) and combined with DNA (deoxyribonucleic acid), and also remarkably inhibiting the DNA damage repairing function of APE1, so that the invention provides the application of gossypol in preparing an APE1 reduction-oxidation inhibitor or a DNA damage repairing function inhibitor of APE1. Furthermore, gossypol can be used for improving the sensitivity of tumor cells to etoposide chemotherapy, and can also reverse drug resistance of the tumor cells to chemotherapeutic medicines caused by high expression of APE1 in the tumor cells, so that the invention also provides application of gossypol in preparing adjuvants or chemosensitizer for treating cancers.

The invention discloses application of a GBE1 inhibitor flavopiridol and its pharmaceutical composition in preparing a medicine for treating lung adenocarcinoma. According to the invention, it is found that flavopiridol can effectively inhibit the proliferation of lung adenocarcinoma cells, and the dose-dependent and time-dependent effects are obvious. According to the results of WB and Moleculardocking, flavopiridol may play a role in inhibiting the proliferation of lung adenocarcinoma cells by inhibiting GBE1, and flavopiridol may be an effective GBE1 inhibitor. Schisandrone alcohol, a compound that may participate in the regulation of GBE1 pathway, cannot directly inhibit the proliferation of lung adenocarcinoma cells, but can enhance the sensitivity of lung adenocarcinoma cells to chemotherapy of flavopiridol. Therefore, flavopiridol and Schisandrone alcohol can be used as a pharmaceutical composition to prepare an anti lung adenocarcinoma pharmaceutical preparation for the treatment of lung adenocarcinoma.

The p53 messenger RNA nanoparticles, a preparation method thereof and an application thereof in preparing a drug for treating tumors belong to the technical field of genetic engineering. The p53 messenger RNA nanoparticles are prepared by the following method: 1, chemically modified p53mRNA is synthesized in vitro; and 2, a nano-system is prepared by a self-assembly method to deliver the p53 messenger RNA in vivo. The p53 messenger RNA nanoparticles play an anti-tumor and chemosensitivity-enhancing therapeutic role by restoring the anti-tumor function of p53. The advantages of the invention are as follows: 1, the p53 messenger RNA in the invention is successfully delivered to the p53 inactivated liver cancer and lung cancer tumor cells through the nano-system to effectively and rapidly induce cell apoptosis and G1 phase cell cycle arrest in vivo and in vitro, thus significantly inhibiting the growth of tumor cells; and 2, the p53 messenger RNA delivered by the nanoparticles can enhancethe anti-tumor effect of a mTOR inhibitor everolimus by supplementing the tumor suppressor p53 deleted in the tumor.

The invention discloses a tumor suppressor gene NDRG2 based application for improving breast cancer chemotherapy sensibility. The tumor suppressor gene NDRG2 is transfected into a breast cancer cell through an expression vector or a virus vector, and the result shows that the tumor suppressor gene NDRG2 can improve the breast cancer chemotherapy sensibility and can be applied to preparation of relevant drugs. The NDRG2 prompts a deoxyribonucleic acid (DNA) damage ability of Adr induced p53 wild type breast cancer cells, improves morphology damage of Adr to p53 wild type breast cancer cells, improves a proliferation inhibiting ability of the Adr to the p53 wild type breast cancer cells, improves the breast cancer chemotherapy sensibility which is independent of specific chemotherapy drugs and further prompts apoptosis of the Adr induced p53 wild type breast cancer cells.

MiR-22 can realize the targeting negative regulation of the expression of REDD1, and the miR-22 is under-expressed in bladder cancer tissues. The miR-22 can influence the sensitivity of bladder cancer cells to paclitaxel chemotherapy through the "REDD1-autophagy" regulation axis, so the miR-22 can be used as a potential target for bladder cancer chemosensitization, and can be used in the preparation of the bladder cancer chemosensitization treatment drugs as the target site, and especially the miR-22 can be used for preparing drugs for inhibiting autophagy and increasing the sensitivity of bladder cancer cells to paclitaxel chemotherapy as the target site. The bladder cancer is BUC.

The invention discloses a radix scutellariae soup, and application of an equivalent component group of the radix scutellariae soup to improvement of the chemosensitivity of the colon cancer on the irinotecan. The invention finds that the radix scutellariae soup can be beneficial to remarkably improving the chemosensitivity of the colon cancer on the irinotecan, namely, improving the killability ofthe irinotecan on the the colon cancer, the inhibiting effect on colon cancer cell proliferation, and the acceleration on colon cancer cell apoptosis, so that without remarkably reducing a chemotherapeutic effect of the irinotecan, the administration dosage of the irinotecan is reduced favorably, and the chemotherapy side effects of the irinotecan is relieved. The invention finds that through a composition prepared from gallic acid, scutellarin, baicalein, wogonin, glycyrrhizic acid and oroxylin A in the radix scutellariae soup, the chemosensitivity of the colon cancer on the irinotecan can be remarkably improved, and the medicine effect is basically consistent to the equivalent dosage of radix scutellariae soup; the find is helpful to develop a composition medicine with definite development components and controllable quality so as to replace the radix scutellariae soup for assisting colon cancer chemotherapy, and also helpful to adopt the composition as a quality control index to control the quality of the radix scutellariae soup.

The invention discloses an application method of long-chain non-coding RNA LOC107987064, a detection preparation and a treatment preparation. The invention relates to a detection reagent for detecting ovarian cancer platinum chemotherapy tolerance, in particular to a kit for detecting whether ovarian cancer is tolerant to platinum drugs or not by a real-time fluorescence quantitative analysis method and a human ovarian cancer platinum tolerance treatment preparation. The researches prove that the LncRNA LOC107987064 is highly expressed in a platinum-resistant ovarian cancer tissue, and the LOC107987064 is a marker of the platinum resistance of the ovarian cancer, so that the expression of the LOC107987064 is applied to the detection of the platinum chemotherapy resistance of the ovarian cancer and the enhancement of the chemotherapy sensitivity of the human ovarian cancer platinum drugs through inhibition, and the LncRNA LOC107987064 has profound clinical significance and generalization performance.

The invention discloses a YAP1 gene and application of an inhibitor in enhancing chemosensitivity of a stem cell of bladder cancer. The YAP1 gene is related to chemosensitivity of the stem cell of bladder cancer. The inhibitor where the YAP1 gene is highly expressed can improve the chemosensitivity of the stem cell of bladder cancer on chemotherapeutics mitomycin C and cis-platinum by down-regulating the expression of the YAP1 gene, so that the inhibiting rate of the chemotherapeutics mitomycin C and cis-platinum on the stem cell of bladder cancer is increased. The inhibitor where the YAP1 gene is highly expressed can be any one or more of siRNA, shRNA, dsRNA, miRNA, cDNA, a small molecular compound, a peptide and an antibody, wherein the small molecular compound is a 2-amido benzoxazole derivative.