Lai Jiang, Jun Qian, Yongbo Yang, Yongtian Fan
Department of Colorectal Surgery, Zhejiang Cancer Hospital, Hangzhou, Zhejiang, China (mainland)
Med Sci Monit 2018; 24:7710-7718
Colon cancer is one of the most common cancers in the world. We performed the present study to determine the molecular mechanism of MON1B in colon cancer cells.
MATERIAL AND METHODS: Colon cancer tissues and adjacent normal tissues were collected from 34 colon cancer patients. MON1B-silenced LoVo colon cancer cells were constructed. RT-qPCR and Western blot analysis were used to detect mRNA and protein levels, respectively, of colon cancer tissues and cells. Cell counting kit-8 (CCK-8), wound healing, and Transwell assays were used to detect viability, migration, and invasion, respectively, of colon cancer cells.
RESULTS: The mRNA and protein levels of MON1B were higher in colon cancer tissues and human colon cancer cell lines (HT-29, SW480, COLO205, LoVo). Cell proliferation, migration, and invasion abilities were all inhibited when MON1B was silenced in LoVo colon cancer cells. Both the mRNA and protein levels of tissue inhibitor of metalloproteinase (TIMP)-2 and iκB were increased, while that of matrix metalloproteinases (MMP)-2, MMP-9, metastasis-associated genes (MTA)-1, nuclear factor-kappa B (NF-κB), and chemokine receptor type (CXCR)-4 was decreased when MON1B was silenced.
CONCLUSIONS: MON1B interference exerted anti-tumor effect in colon cancer in vitro.
Keywords: Colonic Neoplasms, Neoplasm Metastasis, Receptor Activator of Nuclear Factor-kappa B