UBAP2L silencing inhibits cell proliferation and G2/M phase transition in breast cancer

Background Ubiquitin-associated protein 2-like (UBAP2L) contains a ubiquitin-associated domain near its N-terminus, which has been demonstrated to be overexpressed in multiple tumors, including hepatocellular carcinoma and colorectal carcinoma but its role has not been well studied in breast cancer....

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Published in:Breast cancer (Tokyo, Japan) Japan), 2018-03, Vol.25 (2), p.224-232
Main Authors: He, Jing, Chen, Yuanping, Cai, Lu, Li, Zelei, Guo, Xiaoqing
Format: Article
Language:English
Subjects:
Breast cancer
Cancer
Cancer Research
Colorectal cancer
Medicine
Medicine & Public Health
Oncology
Oncology, Experimental
Original
Original Article
Surgery
Surgical Oncology
Ubiquitin
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Summary:Background Ubiquitin-associated protein 2-like (UBAP2L) contains a ubiquitin-associated domain near its N-terminus, which has been demonstrated to be overexpressed in multiple tumors, including hepatocellular carcinoma and colorectal carcinoma but its role has not been well studied in breast cancer. Thus, this study was designed to evaluate whether UBAP2L can serve as a potential molecular target for breast cancer therapy. Methods The expression of UBAP2L was determined in breast cancer tissues and cell lines by Western blotting and Oncomine database mining. Then the expression of UBAP2L was silenced using RNA interference and the effects of UBAP2L knockdown on breast cancer cell proliferation and cell cycle progression by MTT and colony formation assay, and Flow cytometry, respectively. Results We found the expression of UBAP2L was significantly up-regulated in breast cancer tissues and cell lines. Knockdown of UBAP2L suppressed cell proliferation, impaired colony formation ability and induced cell cycle arrest at G2/M phase. At molecular levels, knockdown of UBAP2L increased p21 expression, but decreased the expression of CDK1 and Cyclin B1 in breast cancer cells. Conclusion Our findings suggest that UBAP2L plays an important role in breast cancer cell proliferation and might serve as a potential target for breast cancer treatment.
ISSN:1340-6868
1880-4233
DOI:10.1007/s12282-017-0820-x