Open Access

ARTICLE

Knockdown of REV7 Inhibits Breast Cancer Cell Migration and Invasion

Liu Feng^*†, Wang Wei^*, Zhang Heng^†, Han Yantao^‡, Wang Chunbo^‡

* Medical College, Qingdao University, Qingdao, China
† Pharmaceutical Department, Qingdao Hiser Medical Center, Qingdao, China
‡ Department of Pharmacology, Medical College, Qingdao University, Qingdao, China

Oncology Research 2016, 24(5), 315-325. https://doi.org/10.3727/096504016X14666990347590

Abstract

REV7 (also known as MAD2L2) is a multifunctional protein involved in DNA damage tolerance, cell cycle regulation, gene expression, and carcinogenesis. Although its expression is reportedly associated with poor prognosis in several kinds of human cancers, the significance of REV7 expression in breast malignancies is unclear. In this study, REV7 was found to be increased in breast cancer. We found that knockdown of REV7 inhibited the migration, invasion, and epithelial–mesenchymal transition (EMT) of breast cancer cells. Meanwhile, overexpression of REV7 promoted the migration, invasion, and EMT of breast cancer cells. As shown by Western blot, knockdown of REV7 can promote TGF-β1 expression. Western blot analysis indicated that TGF-β1 may play a role as a downstream factor of REV7. Moreover, interference of TGF-β1 can also inhibit the cell’s ability for migration, invasion, and EMT, as well as in a cell line whose REV7 is overexpressed. Taken together, these results contributed to a recognition of the oncogene functions of REV7 in breast cancer cells and provided a novel direction to treat breast cancer.

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Keywords

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