Wu Bin, Yu Chunli, Zhou Bin, Huang Tingting, Gao Lei, Liu Tao, Yang Xingsheng
Department of Gynecology, Qilu Hospital, Shandong University, Jinan, Shandong 250012, P.R. China.
Department of Gynecology, Taian City Central Hospital, Taian, Shandong 271000, P.R. China.
Exp Ther Med. 2017 Sep;14(3):1947-1952. doi: 10.3892/etm.2017.4788. Epub 2017 Jul 12.
Human trophoblastic cell-surface marker, tumor-associated calcium signal transducer 2 (TROP2), is a newly identified marker that has a vital role in the proliferation and invasion of various tumors. However, its specific function in ovarian cancer has not been researched. The purpose of the present study was to investigate the role of TROP2 in the formation of ovarian cancer and its possible mechanism. TROP2 was knocked down by small interfering (si)RNA in ovarian cancer cell line, A2780. The expression of TROP2 protein following transfection was detected by western blot analysis. Cell viability was determined using a Cell Counting kit-8. Cancer cell migration and invasion were examined by wound healing and cell invasion assays, respectively. Apoptosis-related proteins, such as B-cell lymphoma 2 (Bcl-2) and Bcl-2-associated X protein (Bax), were measured by western blotting. Results demonstrated that the expression levels of TROP2 were markedly downregulated by siRNA in A2780 cells compared with the control groups, which led to strong inhibition of proliferation and invasion. Furthermore, TROP2 downregulation also reduced cell migratory ability. Additionally, in the TROP2-knockout group, Bcl-2 was downregulated and Bax was upregulated compared with the control. The present study suggested that the expression of TROP2 was related to cellular proliferation, migration and invasion. TROP2 may disrupt the balance in the Bax family to participate in apoptosis regulation in A2780 cells. Therefore, the overexpression of TROP2 may have a crucial role in tumorigenesis and tumor progression by disturbing the Bax/Bcl-2 balance in ovarian cancer.
人滋养层细胞表面标志物肿瘤相关钙信号转导蛋白2（TROP2）是一种新发现的标志物，在各种肿瘤的增殖和侵袭中起重要作用。然而，其在卵巢癌中的具体功能尚未得到研究。本研究的目的是探讨TROP2在卵巢癌形成中的作用及其可能机制。在卵巢癌细胞系A2780中，通过小干扰（si）RNA敲低TROP2。转染后通过蛋白质印迹分析检测TROP2蛋白的表达。使用细胞计数试剂盒-8测定细胞活力。分别通过伤口愈合试验和细胞侵袭试验检测癌细胞的迁移和侵袭能力。通过蛋白质印迹法检测凋亡相关蛋白，如B细胞淋巴瘤2（Bcl-2）和Bcl-2相关X蛋白（Bax）。结果表明，与对照组相比，A2780细胞中TROP2的表达水平被siRNA显著下调，这导致增殖和侵袭受到强烈抑制。此外，TROP2下调也降低了细胞迁移能力。另外，在TROP2敲除组中，与对照组相比，Bcl-2下调而Bax上调。本研究表明，TROP2的表达与细胞增殖、迁移和侵袭有关。TROP2可能通过破坏Bax家族的平衡参与A2780细胞的凋亡调节。因此，TROP2的过表达可能通过扰乱卵巢癌中的Bax/Bcl-2平衡在肿瘤发生和肿瘤进展中起关键作用。
