Oncogenic potential of TSTA3 in breast cancer and its regulation by the tumor suppressors miR-125a-5p and miR-125b
Oncogenic potential of TSTA3 in breast cancer and its regulation by the tumor suppressors miR-125a-5p and miR-125b
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DOI：
10.1007/s13277-015-4178-4
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发表时间：
2016-04-01
期刊：
影响因子：
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通讯作者：
Jin, Feng
中科院分区：
文献类型：
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作者：
Sun, Yanan;Liu, Xiaohong;Jin, Feng
TSTA3参与酶代谢并影响糖基化过程，糖基化异常影响细胞的恶性转化和肿瘤的发展。然而，研究尚未检测TSTA3在乳腺癌（BC）中的分子生物学功能。检测TSTA3在BC组织和细胞系中的表达。Kaplan-Meier生存试验和Cox回归分析预后。利用TSTA3缺失分析细胞功能。预测TSTA3的上游mirna，并使用RT2 Profiler (TM) PCR阵列分析下游靶基因。我们的研究结果表明，TSTA3在BC组织和细胞中高表达，并与低生存率相关。TSTA3的表达与TNM状态相关（P < 0.01），是独立的预后因素（P = 0.041）。TSTA3-siRNA降低体外细胞侵袭和增殖。miR-125a-5p和miR-125b是TSTA3的上游靶点，PCR阵列显示TSTA3影响CXCR4-CXCL12基因。研究结果表明，miR-125a-5p/miR-125b抑制TSTA3的表达，TSTA3通过调节CXCR4的表达来控制细胞增殖和侵袭。综上所述，TSTA3的高表达在癌变过程中具有原癌作用，可作为BC患者的独立分子标志物。
TSTA3 participates in enzyme metabolism and affects glycosylation processes, and abnormal glycosylation influences the malignant transformation of cells and tumor development. However, studies have not examined the molecular biological function of TSTA3 in breast cancer (BC). The expression of TSTA3 was examined in BC tissues and cell lines. Kaplan-Meier survival tests and Cox regression were used to analyze prognosis. TSTA3 depletion was used to analyze cell function. The upstream miRNAs of TSTA3 were predicted, and the downstream target gene was analyzed using a RT2 Profiler (TM) PCR array. Our results show that TSTA3 was highly expressed in BC tissues and cells and was correlated with poor survival. The expression of TSTA3 was correlated with the TNM status (P < 0.01) and served as an independent prognostic factor (P = 0.041). TSTA3-siRNA decreased cell invasion and proliferation in vitro. miR-125a-5p and miR-125b are upstream targets of TSTA3, and a PCR array revealed that TSTA3 affects the CXCR4-CXCL12 genes. The findings suggest that miR-125a-5p/miR-125b suppress the expression of TSTA3, which controls cell proliferation and invasion by regulating CXCR4 expression. In conclusion, a high expression of TSTA3 exerts a proto-oncogenic effect during carcinogenesis and serves as an independent molecular marker for BC patients.