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©2013 Baishideng Publishing Group Co.
World J Gastroenterol. May 21, 2013; 19(19): 2913-2920
Published online May 21, 2013. doi: 10.3748/wjg.v19.i19.2913
Published online May 21, 2013. doi: 10.3748/wjg.v19.i19.2913
Figure 2 The effect on molecular by overexpression of p42.
3 in HepG2 cells. A: Reverse transcription-polymerase chain reaction and Western blotting were performed to confirm p42.3 overexpression in a stable single colony of HepG2-p42.3-1 and HepG2-p42.3-2 cells. p42.3 expression was deficient in the HepG2-vector control cells. β-actin served as an internal control; B: Expression of proteins shown as mean ± SD. Consistent with p42.3 protein expression, proliferating cell nuclear antigen (PCNA), mitotic arrest deficient 2 (MAD2) and cyclin B1 expression were significantly upregulated. The protein levels of cell division cycle 25 A (Cdc25A) and cell division cycle 25 homolog C (Cdc25C) hardly changed following p42.3 expression (bP < 0.01 vs HepG2-vector).
- Citation: Sun W, Dong WW, Mao LL, Li WM, Cui JT, Xing R, Lu YY. Overexpression of p42.3 promotes cell growth and tumorigenicity in hepatocellular carcinoma. World J Gastroenterol 2013; 19(19): 2913-2920
- URL: https://www.wjgnet.com/1007-9327/full/v19/i19/2913.htm
- DOI: https://dx.doi.org/10.3748/wjg.v19.i19.2913