Chemotherapy is one of the most important treatments for cancer therapy. However, chemotherapy resistance is a big challenge in cancer treatment. Due to chemotherapy resistance, drugs become less effective or no longer effective at all. In recent years, long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) has been found to be associated with the development of chemotherapy resistance, suggesting that MALAT1 may be an important target to overcome chemotherapy resistance. In this review, we introduced the main mechanisms of chemotherapy resistance associated with MALAT1, which may provide new approaches for cancer treatment.
Purpose DARS antisense RNA 1 (DARS-AS1) is a long non-coding RNA that has been validated as a critical regulator in several human cancer types. Our study aimed to determine the expression profile of DARS-AS1 in prostate cancer (PCa) tissues and cell lines. Functional experiments were conducted to explore the detailed roles of DARS-AS1 in regulating PCa carcinogenesis. Furthermore, the detailed mechanisms by which DARS-AS1 regulates the oncogenicity of PCa cells were uncovered. Methods Reverse transcription quantitative polymerase chain reaction was performed to analyze DARS-AS1 expression in PCa tissues and cell lines. Cell Counting Kit-8 assays, flow cytometry analyses, Transwell assays, and tumor xenograft experiments were conducted to determine the regulatory effects of DARS-AS1 knockdown on the malignant phenotype of PCa cells. Bioinformatics analysis was performed to identify putative microRNAs (miRNAs) targeting DARS-AS1, and the direct interaction between DARS-AS1 and miR-628-5p was verified using RNA immunoprecipitation and luciferase reporter assays. Results DARS-AS1 was highly expressed in PCa tissues and cell lines. In vitro functional experiments demonstrated that DARS-AS1 depletion suppressed PCa cell proliferation, promoted cell apoptosis, and restricted cell migration and invasion. In vivo studies revealed that the downregulation of DARS-AS1 inhibited PCa tumor growth in nude mice. Mechanistic investigation verified that DARS-AS1 functioned as an endogenous miR-628-5p sponge in PCa cells and consequently promoted the expression of metadherin (MTDH). Furthermore, the involvement of miR-628-5p/MTDH axis in DARS-AS1-mediated regulatory actions in PCa cells was verified using rescue experiments. Conclusion DARS-AS1 functioned as a competing endogenous RNA in PCa by adsorbing miR-628-5p and thereby increasing the expression of MTDH, resulting in enhanced PCa progression. The identification of a novel DARS-AS1/miR-628-5p/MTDH regulatory network in PCa cells may offer a new theoretical basis for the development of promising therapeutic targets.
Background. Sinomenine has been reported to effectively repress the progression of lung cancer and breast cancer. However, the effects of sinomenine in bladder cancer are not well understood. The purpose of this study was to evaluate the effects of sinomenine in bladder cancer. Methods. The mRNA expression of HEIH in bladder cancer cells was measured by RT-qPCR. T24 and SW780 cells were treated with sinomenine for 24 hours. Cell viability was detected by the MTT assay. Cell migration and invasion were detected by the transwell assay. Western blotting assay was performed to assess the protein expression of Bcl-2, Bax, and caspase-3. Results. Sinomenine significantly suppressed cell viability in T24 and SW780 cells. Moreover, cell migration and invasion were significantly inhibited by sinomenine. Sinomenine accelerated the expression of Bax and caspase-3 but decreased the expression of Bcl-2. HEIH was upregulated in bladder cancer cells compared with normal bladder epithelial cells. Besides this, we noticed that HEIH knockdown blocked cell proliferation, migration, and invasion but facilitated cell apoptosis in bladder cancer cells. Additionally, HEIH reversed the suppression of the progression induced by sinomenine. Conclusion. Sinomenine was observed to suppress cell progression of bladder cancer cells by inhibiting HEIH expression. Our findings suggested that the use of sinomenine might be an effective treatment for bladder cancer.
Background: Basement membrane (BM) genes are an important factor in the process of clear cell renal cell carcinoma (ccRCC). Thus, identifying BMs with prognostic values in ccRCC is critical. Methods: The samples from TCGA were separated randomly into 2 cohorts, the training cohort, and the validation cohort. For the training cohort univariate Cox, Lasso, and multivariate Cox regression analyses were applied to identify prognostic BM genes and then construct a prognostic BM-genes’ signature. The nomogram was applied to predict prognosis at different clinicopathological stages and risk scores. GO and KEGG analyses were applied to the differentially expressed genes. Moreover, the CIBERSORT and ESTIMATE scores were calculated and compared between the high-risk cohort and the low-risk cohort. Results: A prognostic risk model of four BM genes, including ADAMTS14, COL7A1, HSPG2, and TIMP3, was constructed. There were also significant differences in survival time between the high-risk and low-risk groups for the validation cohort and the entire cohort. The risk model was validated as a new independent prognostic factor for ccRCC by univariate and multivariate Cox regression together with clinicopathological characteristics. In addition, a nomogram showed good prediction. The model can also analyze the possibility of immune escape and response to immunotherapy in ccRCC patients. In addition, the results of a pan-cancer analysis showed that these four model genes were associated with immune-related genes in a variety of cancers. Conclusion: The signature of four BM genes had a significant prognostic value for ccRCC. They may be promising targets for therapy, especially immune therapy.
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