MicroRNA-21-mediated regulation of Sprouty2 protein expression enhances the cytotoxic effect of 5-fluorouracil and metformin in colon cancer cells.

Abstract	Sprouty2 (Spry2) was identified recently as a tumor suppressor gene in cancer cells which inhibits the activation of receptor tyrosine kinases (RTKs). The present study explored the effect of Spry2 in colon cancer cells in order to assess its potential use in the treatment of colon cancer. Expression of Spry2 inhibited the growth of a colon cancer cell line, HCT116, and induced sensitization to fluorouracil (5-FU) and metformin. Spry2 promoted apoptosis of cancer cells in association with activation of the phosphatase and tensin homolog deleted on chromosome 10 (PTEN) pathway and the blockade of Ras-Raf-Erk signaling. Treatment of Spry2-HCT116 cells with metformin resulted in a more prominent effect on the inhibition of cell migration. Inhibition of microRNA-21 (mir‑21) induced upregulation of Spry2 and PTEN which underscores the importance of mir-21 in Spry2-associated tumorigenesis of the colon. These results point toward a potential strategy for colon cancer treatment worthy of further investigation.
Authors	Yin-Hsun Feng, Chao-Liang Wu, Ai-Li Shiau, Jenq-Chang Lee, Jan-Gowth Chang, Pei-Jung Lu, Chao-Ling Tung, Li-Yia Feng, Wen-Tsung Huang, Chao-Jung Tsao
Journal	International journal of molecular medicine (Int J Mol Med) Vol. 29 Issue 5 Pg. 920-6 (May 2012) ISSN: 1791-244X [Electronic] Greece
PMID	22322462 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References	Antimetabolites, Antineoplastic Hypoglycemic Agents Intracellular Signaling Peptides and Proteins MIRN21 microRNA, human Membrane Proteins MicroRNAs SPRY2 protein, human Metformin PTEN Phosphohydrolase Fluorouracil
Topics	Antimetabolites, Antineoplastic (pharmacology) Cell Movement Cell Proliferation Colonic Neoplasms (drug therapy, genetics, metabolism) Fluorouracil (pharmacology) Gene Expression Regulation, Neoplastic HCT116 Cells Humans Hypoglycemic Agents (pharmacology) Intracellular Signaling Peptides and Proteins (genetics, metabolism) Membrane Proteins Metformin (pharmacology) MicroRNAs (genetics, metabolism) PTEN Phosphohydrolase (genetics, metabolism) Up-Regulation

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