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TRIM14 Promotes Breast Cancer Cell Proliferation by Inhibiting Apoptosis

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Department of General Surgery, Shanghai Traditional Chinese Medicine-Integrated Hospital, Shanghai, P.R. China

Oncology Research 2019, 27(4), 439-447. https://doi.org/10.3727/096504018X15214994641786

Abstract

Tripartite motif-containing 14 (TRIM14) is abnormally expressed in several human cancers. However, the function and expression of TRIM14 in human breast cancer are still largely unknown. To understand the biological function of TRIM14 in breast cancer, we measured the expression level of TRIM14. Cell proliferation and cell apoptosis were measured after TRIM14 overexpression or knockdown. Upregulation of TRIM14 was found in human breast cancer specimens and cell lines. Reduction of TRIM14 inhibited cell proliferation but increased cell apoptosis in the BT474 and MDA-MB-231 cell lines. Further study showed that knockdown of TRIM14 upregulated the expression of BAX while downregulating the expression of BCL2. In addition, the expression of SHP-1 was increased, and the phosphorylation of STAT3 (p-STAT3) was inhibited. Conversely, overexpression of TRIM14 had the opposite effects. Additionally, cryptotanshinone, a STAT3 inhibitor, inhibited cell proliferation but increased cell apoptosis in the BT474 and MDA-MB-231 cell lines. In conclusion, TRIM14 may act as an oncogene in human breast cancer and may be a novel strategy for human breast cancer.

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APA Style
Hu, G., Pen, W., Wang, M. (2019). TRIM14 promotes breast cancer cell proliferation by inhibiting apoptosis. Oncology Research, 27(4), 439-447. https://doi.org/10.3727/096504018X15214994641786
Vancouver Style
Hu G, Pen W, Wang M. TRIM14 promotes breast cancer cell proliferation by inhibiting apoptosis. Oncol Res. 2019;27(4):439-447 https://doi.org/10.3727/096504018X15214994641786
IEEE Style
G. Hu, W. Pen, and M. Wang, “TRIM14 Promotes Breast Cancer Cell Proliferation by Inhibiting Apoptosis,” Oncol. Res., vol. 27, no. 4, pp. 439-447, 2019. https://doi.org/10.3727/096504018X15214994641786



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This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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