4.4 Article

BTG1 potentiates apoptosis and suppresses proliferation in renal cell carcinoma by interacting with PRMT1

Journal

ONCOLOGY LETTERS
Volume 10, Issue 2, Pages 619-624

Publisher

SPANDIDOS PUBL LTD
DOI: 10.3892/ol.2015.3293

Keywords

renal cell carcinoma; B-cell translocation gene 1; protein arginine N-methyltransferase 1; cell cycle; apoptosis; proliferation

Categories

Funding

  1. National Natural Science Foundation of China [81370849, 81300472, 81202034]
  2. Natural Science Foundation of Jiangsu Province [BL2013032, BK20112336]
  3. Nanjing City [201201053]
  4. Southeast University [3290002402]
  5. Science Foundation of Ministry of Education of China [20120092120071]

Ask authors/readers for more resources

B-cell translocation gene 1 (BTG1) is a member of the BTG/transducer of Erb family. BTG1 regulates cell cycle progression, inhibits proliferation, promotes apoptosis and stimulates cellular differentiation in multiple cell types. However, the functions of BTG1 in renal cell carcinoma (RCC) remain unclear. Therefore, the present study investigated the role of BTG1 in RCC tissue samples and 786-O RCC cells. RCC tissues and cells exhibited significantly weaker BTG1 protein and mRNA expression compared with para-carcinoma control tissues (P<0.05). Upregulated BTG1 expression induced significant G0/G1 cell cycle arrest, apoptosis and inhibition of cell proliferation in 786-O cells (P<0.05). Furthermore, BTG1 interacted with protein arginine N-methyltransferase 1 (PRMT1), and blocking the action of PRMT1 in 786-O cells resulted in inhibition of BTG1 function. These findings indicate that BTG1 may inhibit cell growth and promote apoptosis by interacting with PRMT1 in RCC; the identification of this mechanism may aid in the production of novel therapies for RCC.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.4
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available