The long noncoding RNA cancer susceptibility 9 (CASC9) has been reported to be a pivot modulator in growth and metastasis of breast cancer, liver cancer, esophageal squamous cell carcinoma, lung adenocarcinoma, gastric cancer, and nasopharyngeal cancer. However, its potential roles in ovarian cancer remain unclear. In this study, we aimed at its functions and molecular mechanism in ovarian cancer progression. We showed that CASC9 was highly expressed in ovarian cancer tissues and cell lines. An elevated level of CASC9 predicts an unfavorable prognosis in patients with ovarian cancer. Loss‐of‐function and gain‐of‐function assays illustrated that CASC9 promotes ovarian cancer cell proliferation, migration, and invasion in vitro, and accelerates tumor growth in vivo. We showed that CASC9 works as a competing endogenous RNA (ceRNA) for miR‐758‐3p which targets LIN7A. CASC9 inhibits the level of miR‐758‐3p, and in turn stimulates LIN7A expression in ovarian cancer. Overexpression of LIN7A reverses the suppressive roles of CASC9 depletion on ovarian cancer. In sum, our findings reveal a novel undefined regulatory signaling pathway, namely CASC9/miR‐758‐3p/LIN7A axis, involved in ovarian cancer progression.
FAM83D has been demonstrated to contribute to tumorigenesis. However, its immune effects in hepatocellular carcinoma (HCC) have not been reported. This study aimed to identify the immune role of FAM83D in HCC. FAM83D was over-expressed in HCC and contributed to poor prognosis according to the results of data analysis based on The Cancer Genome Atlas (TCGA). Afterward, the levels of immune cells infiltration were found to be correlated with the expression level of FAM83D in HCC. Through TISIDB and cBioPortal network tools, a total of 82 FAM83D-associated genes were screened out, including 12 immunoinhibitors, 20 immunostimulators and 50 tightly co-expressed genes. TCGA cohort was divided into train set and test set on the basis of the proportion of 7:3. According to FAM83D-associated immunomodulators, a four gene predicted model was established using train set via the Cox regression analysis. Survival analysis demonstrated that the overall survival (OS) of high-risk HCC patients was poor compared with the patients in low-risk group. The reliability and predicted power of the risk-score model were identified by a receiver operating characteristic (ROC) curve. A risk-score based nomogram as well as a calibration curve, which were created could be used to anticipate patient's 1-year, 3-year and 5-year survival probabilities. The test set was used to validate these results. Our findings showed that the FAM83D gene was related with HCC immunity. The immune marker chosen could be a promising biomarker for HCC prognosis.
Small-cell lung cancer (SCLC) represents the progressive form of lung cancer.
Patients with SCLC have poor prognosis, partially due to drug resistance.
Therefore, understanding the underlying mechanism for drug resistance in SCLC is
needed to improve clinical outcomes. The concentrations of heat shock protein
90α (HSP90α) in medium were detected by enzyme-linked immunosorbent assay. The
protein levels were detected by Western blot. Cell apoptosis was detected by
propidium iodide staining in cell lines or terminal deoxynucleotidyl transferase
dUTP nick end labeling staining in tumor sections. Doxorubicin (DOX) was
administered into cultured cell lines or intraperitoneally injected into
xenograft mouse to induce apoptosis. In SCLC cell lines, either DOX or ABT-737
increased extracellular HSP90α levels, which attenuated the percentage of
apoptotic cells. Extracellular HSP90α activated Ak strain transforming (AKT) and
β-catenin signaling and inhibited glycogen synthase kinase 3β (GSK3β) signaling.
In the xenograft mouse model, extracellular HSP90α promoted tumor development
and inhibited apoptosis of tumor cells. Heat shock protein 90α attenuates the
efficacy of anticancer drugs in SCLC cells through AKT/GSK3β/β-catenin
signaling.
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