期刊
GENE
卷 715, 期 -, 页码 -出版社
ELSEVIER
DOI: 10.1016/j.gene.2019.144015
关键词
TRIM13; Apoptosis; NF-kappa B
资金
- Scientific Program of Changzhou [CJ20180029, ZD201602, CE20185045]
- Scientific Program of Shandong Provincial Department of Education [J18KA254]
Tripartite Motif Containing 13 (TRIM13), a member of TRIM proteins, is deleted in multiple tumor types, especially in B-cell chronic lymphocytic leukemia and multiple myeloma. The present study explored the expression and potential role of TRIM13 in non-small-cell lung carcinoma (NSCLC). We found that TRIM13 mRNA and protein expression was reduced in NSCLC tissues and cell lines in comparison to paired non-cancerous tissues and a human normal bronchial epithelial cell line, respectively. Overexpression of TRIM13 in NCI-H1975 and SPC-A-1 cells hampered cell proliferation. Additionally, TRIM13 overexpression increased the levels of cleaved caspase-3. TRIM13-induced NSCLC cell apoptosis was attenuated by a caspase-3 inhibitor Ac-DEVD-CHO, suggesting that TRIM13 induced cell apoptosis partially through a caspase-3-dependent pathway. Moreover, it has been reported that TRIM13 can regulate nuclear factor kappaB (NF-kappa B) activity. Our data showed that TRIM13 overexpression inactivated NF-kappa B as indicated by the increased cytosolic NF-kappa B and decreased nuclear NF-kappa B. Exposure to an NF-kappa B inhibitor PDTC significantly blocked the impact of TRIM13 knockdown on cell proliferation and apoptosis, indicating the functions of TRIM13 in NSCLC cells were mediated by the NF-kappa B pathway. Finally, we demonstrated that TRIM13 overexpression suppressed tumor growth and induced cell apoptosis in vivo by using a xenograft mouse model. Collectively, our results indicate that TRIM13 behaves as a tumor suppressor in NSCLC through regulating NF-kappa B pathway. Our findings may offer a promising therapeutic target for NSCLC.
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