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eISSN: 1643-3750

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ALG3 Is Activated by Heat Shock Factor 2 and Promotes Breast Cancer Growth

Yongde Yang, Yanlin Zhou, Xin Xiong, Man Huang, Xueyan Ying, Mengyuan Wang

(Department of Breast Diseases, Chongqing Three Gorges Central Hospital, Chongqing, China (mainland))

Med Sci Monit 2018; 24: CLR3479-3487

DOI: 10.12659/MSM.907461


BACKGROUND: Previous research found that ALG3 is associated with cervical cancer, but the role of ALG3 in breast cancer was still unknown.
MATERIAL AND METHODS: The expression of ALG3 in breast carcinoma tissues was determined by immunochemistry. The ability of cellular proliferation, migration, and invasion was determined by CCK-8 assay, wound healing migration assay, and cell invasion assays, respectively. The binding between HSF2 and promoter of ALG3 was determined by ChIP assay.
RESULTS: There was an increased expression of ALG3 in breast cancer tissues compared to normal breast tissues (p<0.05). High expression of ALG3 was significantly correlated with poor OS (p<0.05). ALG3 expression was significantly increased in cancer samples with advanced stages (stage III/IV) compared with those in the early stages of disease (stage I/II) (p<0.05). The staining intensity of ALG3 was significantly correlated to the tumor grade (grades 2–3 versus 1, p<0.05). Silencing ALG3 or HSF2 inhibited the proliferation, migration, and invasion abilities of MCF-7 cells. Silencing ALG3 retarded the growth of MCF-7 cells in vivo.
CONCLUSIONS: Silencing ALG3 inhibited MCF-7 cells growth in vitro and in vivo. HSF2 activated ALG3 and promoted the growth of breast carcinoma.

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