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10.1016/j.ccell.2014.09.015

http://scihub22266oqcxt.onion/10.1016/j.ccell.2014.09.015
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C4269832!4269832!25517751
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suck abstract from ncbi


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pmid25517751      Cancer+Cell 2014 ; 26 (5): 738-53
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  • TRPM3 and miR-204 establish a regulatory circuit that controls oncogenic autophagy in clear cell renal cell carcinoma #MMPMID25517751
  • Hall DP; Cost NG; Hegde S; Kellner E; Mikhaylova O; Stratton Y; Ehmer B; Abplanalp WA; Pandey R; Biesiada J; Harteneck C; Plas DR; Meller J; Czyzyk-Krzeska MF
  • Cancer Cell 2014[Nov]; 26 (5): 738-53 PMID25517751show ga
  • Autophagy promotes tumor growth by generating nutrients from the degradation of intracellular structures. Here we establish, using shRNAs, a dominant negative mutant, and a pharmacologic inhibitor, mefenamic acid (MFA), that the Transient Receptor Potential Melastatin 3 (TRPM3) channel promotes growth of clear cell renal cell carcinoma (ccRCC) and stimulates MAP1LC3A (LC3A) and MAP1LC3B (LC3B) autophagy. Increased expression of TRPM3 in RCC leads to Ca2+ influx, activation of CAMKK2, AMPK, and ULK1, and phagophore formation. In addition, TRPM3 Ca2+ and Zn2+ fluxes inhibit miR-214 which directly targets LC3A and LC3B. The von Hippel-Lindau tumor suppressor (VHL) represses TRPM3 through miR-204 directly and indirectly through another miR-204 target, Caveolin 1 (CAV1).
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