Tumor suppressor p16 inhibits cancer cell growth by downregulating eEF1A2 through a direct interaction
نویسندگان
چکیده
eEF1A2 through a direct interaction Mee-Hyun Lee*, Bu Young Choi*, Yong-Yeon Cho, Sung-Young Lee, Zunnan Huang, Joydeb Kumar Kundu, Myoung Ok Kim, Dong Joon Kim, Ann M. Bode, Young-Joon Surh and Zigang Dong The Hormel Institute, University of Minnesota, MN 55912, USA WCU Department of Molecular Medicine and Biopharmaceutical Sciences, Graduate School of Convergence Science and Technology and Tumor Microenvironment Global Core Research Center, College of Pharmacy, Seoul National University, Seoul, South Korea Pharmaceutical Science and Engineering, School of Convergence Bioscience and Technology, University of SeoWon, Chungju, Chungbuk, 361-742, South Korea College of Pharmacy, The Catholic University of Korea, Bucheon, Gyeonggi-do, South Korea College of Pharmacy, Keimyung University, Daegu, South Korea School of Animal Science, KyungPook National University, Sangju, South Korea
منابع مشابه
Tumor suppressor p16(INK4a) inhibits cancer cell growth by downregulating eEF1A2 through a direct interaction.
The tumor suppressor protein p16(INK4a) is a member of the INK4 family of cyclin-dependent kinase (Cdk) inhibitors, which are involved in the regulation of the eukaryotic cell cycle. However, the mechanisms underlying the anti-proliferative effects of p16(INK4a) have not been fully elucidated. Using yeast two-hybrid screening, we identified the eukaryotic elongation factor (eEF)1A2 as a novel i...
متن کاملMiR-125b inhibits stromal cell proliferation in giant cell tumor of bone by targeting parathyroid hormone 1 receptor
Objective(s):miR-125b has been identified as a tumor suppressor in many tumors, but its role in giant cell tumor (GCT) of bone remains poorly understood. The current study aimed to investigate the potential role and mechanism of miR-125b in GCT. Materials and Methods:Expression levels of miR-125b in GCT tissues were determined using RT-PCR. The cell proliferation was surveyed by direct cell coun...
متن کاملDown-regulation of Human DNA-(Cytosine-5) Methyltransferase Induces Cell Cycle Regulators p16 and p21 by Distinct Mechanisms*
A common event in the development of human neoplasia is the loss of growth regulatory tumor suppressor functions. Methylation of 5* CpG islands of tumor suppressor genes and elevated levels of the DNA-(cytosine5)-methyltransferase enzyme (DNA MeTase) are also prevalent features of human neoplasia. However, direct evidence that elevated DNA MeTase levels alter gene expression and influence oncog...
متن کاملUp-regulation of p16 by miR-877-3p inhibits proliferation of bladder cancer
Despite the recent studies which have shown that microRNA (miRNA) negatively regulates gene expression by silencing the expression of target genes, here we reported the new evidence of microRNA-mediated gene activation by targeting specific promoter sites. We identified a miR-877-3p binding site on the promoter site of tumor suppressor gene p16 which alters frequently in bladder cancer. Enforce...
متن کاملTumor suppressor p16INK4A is necessary for survival of cervical carcinoma cell lines.
The tumor suppressor p16(INK4A) inhibits formation of enzymatically active complexes of cyclin-dependent kinases 4 and 6 (CDK4/6) with D-type cyclins. Oncogenic stress induces p16(INK4A) expression, which in turn triggers cellular senescence through activation of the retinoblastoma tumor suppressor. Subversion of oncogene-induced senescence is a key step during cancer development, and many tumo...
متن کامل