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The impact of TNFSF14 on prognosis and immune microenvironment in clear cell renal cell carcinoma
Fangshi Xu,Yibing Guan,Peng Zhang,Li Xue,Xiaojie Yang,Ke Gao,Tie Chong 한국유전학회 2020 Genes & Genomics Vol.42 No.9
Background TNFSF14 has been proven to play an important role in various types of tumors. However, its function in renal cell carcinoma (RCC) has not yet been fully elucidated. Objective In order to explore molecular mechanism of RCC, we evaluated the efect of TNFSF14 on RCC progression, prognosis and immune microenvironment. Methods Using TCGA database, the diferential expression of TNFSF14 and its relationships between clinicopathological features and prognosis were determined. Cox univariate and multivariate analyses were successively performed to identify whether TNFSF14 was an independent prognostic factor. The discriminating ability of TNFSF14 in RCC prognosis analysis was validated under the same clinical subgroups. Tumor mutational burden (TMB) of each RCC samples was calculated and the diferential expression of TNFSF14 between high- and low-TMB groups was analyzed. The immune abundances of 22 leukocyte subtypes in each RCC samples were presented through the CIBERSORT algorithm. TIMER database was used to explore the relationships between copy number of TNFSF14 and the infltration levels of 6 immune cells. Results Overexpression of TNFSF14 implied adverse clinicopathological features and poor prognosis. Meanwhile, TNFSF14 was identifed as an independent prognostic factor (HR=1.047, P=0.028) and possessed prevalent applicability in RCC prognostic analysis. TNFSF14 was upregulated in high-TMB group than that in low-TMB group (Log2FC=0.722). Moreover, overexpression of TNFSF14 brought alteration of immune abundance of 8 leukocyte subtypes. Besides, somatic copy number alteration (SCNA) of TNFSF14 was associated with infltration levels of 6 immune cells. Conclusions TNFSF14 has crucial impact on progression, prognosis and immune microenvironment in RCC. Besides, TNFSF14 may be a potential biomarker for predicting the efcacy and response rate of RCC immunotherapy.
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RBPJ contributes to acquired docetaxel resistance in prostate cancer cells
Li Xue,Zhenlong Wang,Hecheng Li,Zhaolun Li,Qi Chen,Peng Zhang,Haiwen Chen,Ziming Wang,Tie Chong,T. Chong 대한독성 유전단백체 학회 2017 Molecular & cellular toxicology Vol.13 No.3
Our previous work has shown that depletion of recombination signal-binding protein J (RBPJ) results in reduced cell growth in prostate cancer cells. In this study, we aimed to investigate the function of RBPJ in the chemoresistance of prostate cancer. The expression of RBPJ was quantified in docetaxel-resistant and parental prostate cancer cells. Loss- and gainof- function experiments were conducted to explore the regulatory role of RBPJ in prostate cancer sensitivity to docetaxel. The pro-apoptotic effect of RBPJ silencing was checked in docetaxel-resistant prostate cancer cells. We found that docetaxel-resistant PC3-DR and DU145- DR cells expressed 3-5-fold high levels of RBPJ than parental PC3 and DU145 cells. Short hairpin RNAmediated knockdown of RBPJ inhibited cell proliferation and colony formation and reversed docetaxel resistance in docetaxel-resistant prostate cancer cells. In contrast, overexpression of RBPJ promoted cell growth, colony formation, and docetaxel resistance in parental prostate cancer cells. Downregulation of RBPJ induced apoptosis in docetaxel-resistant cells, which was accompanied by enhanced cleavage of caspase-3. In addition, RBPJ silencing or overexpression markedly modulated the expression of the Bcl-2 family members including Bcl-2, Bcl-xL, Mcl-1, Bax, and Bak. Altogether, RBPJ contributes to acquisition of docetaxel resistance in prostate cancer cells and may thus represent a potential target for overcoming chemotherapeutic resistance in this malignancy.
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