Open AccessN-Myc downstream-regulated gene 2 suppresses proliferation and induces oncosis of OS-RC-2 human renal cancer cells
Author(s) -
Liao Huihua,
Zhou Wu,
Xingduan Huang,
Zhiqing Qiu,
Huien Wu
Publication year - 2014
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2014.2882
Subject(s) - oncogene , cell cycle , flow cytometry , cell growth , biology , apoptosis , cancer cell , cancer research , cell , microbiology and biotechnology , transfection , a431 cells , cancer , cell culture , biochemistry , genetics
V‑myc avian myelocytomatosis viral oncogene homolog (Myc) regulates cell proliferation, differentiation and apoptosis in several types of cancer. N‑myc downstream‑regulated gene 2 (NDRG2) is known to exhibit reduced expression in renal cell carcinoma (RCC) tissues compared with adjacent non‑neoplastic tissues and is an independent poor prognostic factor predicting survival in RCC. In the present study, green fluorescent protein (GFP)‑NDRG2 and control GFP recombinant adenovirus plasmids were constructed and used to infect human renal cancer (OS‑RC‑2) cells. NDRG2 expression was measured using western blot analysis and the subcellular localization of NDRG2 was detected using confocal microscopy. The rate of proliferation of the cells was measured using colony formation and MTT assays, and the cell cycle was analyzed using flow cytometry. The results showed that the OS‑RC‑2 cells expressed little NDRG2 prior to infection with GFP‑NDRG2 recombinant adenovirus; however, following infection, NDRG2 was found to be overexpressed, primarily in the mitochondria. The proliferation rate of the OS‑RC‑2 cells was reduced by NDRG2. Approximately 84.8% of the NDRG2‑expressing cells were in S phase compared with 58.7% in the control virus‑infected cells (P<0.05). In addition, the upregulation of NDRG2 induced a higher proportion of OS‑RC‑2 cells to undergo oncosis instead of apoptosis. In conclusion, the results from this study suggest that NDRG2 expressed in mitochondria may arrest renal cancer cells in S phase, decrease cell proliferation and induce oncosis. This indicates that NDRG2 is not only a biomarker, but may also be a therapeutic target for the treatment of RCC.