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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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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 PMID25517751 show 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 the growth of clear cell renal cell carcinoma (ccRCC) and stimulates MAP1LC3A (LC3A) and MAP1LC3B (LC3B) autophagy. Increased expression of TRPM3 in RCC leads to Ca(2+) influx, activation of CAMKK2, AMPK, and ULK1, and phagophore formation. In addition, TRPM3 Ca(2+) and Zn(2+) fluxes inhibit miR-214, which directly targets LC3A and LC3B. The von Hippel-Lindau tumor suppressor (VHL) represses TRPM3 directly through miR-204 and indirectly through another miR-204 target, Caveolin 1 (CAV1).
  • |*Autophagy [MESH]
  • |Animals [MESH]
  • |Carcinoma, Renal Cell/genetics/metabolism/*pathology [MESH]
  • |Caveolin 1/metabolism [MESH]
  • |Cell Line, Tumor [MESH]
  • |Gene Expression Regulation, Neoplastic [MESH]
  • |HEK293 Cells [MESH]
  • |Humans [MESH]
  • |Kidney Neoplasms/genetics/*pathology [MESH]
  • |Mice, Nude [MESH]
  • |MicroRNAs/*physiology [MESH]
  • |Neoplasm Transplantation [MESH]
  • |Oncogenes [MESH]
  • |RNA Interference [MESH]
  • |TRPM Cation Channels/*genetics/metabolism [MESH]
  • |Tumor Burden [MESH]


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