期刊
FOOD AND CHEMICAL TOXICOLOGY
卷 62, 期 -, 页码 892-900出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.fct.2013.10.028
关键词
Butyrate; ndocan; Colorectal cancer; MAPK; shRNA; Lentivirus
资金
- National Nature Science Research Grants [81272399, 81070232, 81270372]
- Education Ministry Research Grant of Anhui province [KJ2011Z173]
- Key Project of Chinese Ministry of Education [212077]
- Anhui Medical University [2010xkjzj002]
Butyrate is a short-chain fatty acid produced by colonic bacterial fermentation. In colon cancer cells butyrate is able to suppress cell growth, induce apoptosis. It also inhibits tumor growth in vivo. However, the underlying mechanism is still not fully understood. We hypothesize that butyrate regulates the growth and migration of colon cancer cells by altering endocan expression. To test this hypothesis, we performed quantitative real time RT-PCR and Western blots, and found that butyrate increased endocan expression of colon cancer cell RKO. Moreover, endocan over-expression inhibited RICO proliferation, migration and colony formation. Functionally, butyrate significantly suppressed RKO proliferation, migration, and colony formation, as well as induced apoptosis. Knocking down endogenous endocan was able to attenuate the inhibitory role of butyrate in RKO migration and proliferation. Since our results showed that butyrate inhibited MAPK/ERK2 phosphorylation. To determine whether ERK2 signaling is associated with endocan expression, we knocked down endogenous ERK2 expression. Our results showed that knocking down ERK2 expression up-regulated endocan expression. Taken together, these results suggested that butyrate suppressed RK0 proliferation, colony formation, migration through up-regulating endocan expression via ERK2/MAPK signaling pathway. (C) 2013 Elsevier Ltd. All rights reserved.
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