Fig 1: Expression of TGM2, MDM2, and SQSTM1/p62 in RCC: (A) Microarray data from the U.S. National Cancer Institute (http://dtp.nci.nih.gov/mtweb/targetdata). TGM2 (experiment ID: 9993; https://dtp.cancer.gov/mtweb/targetinfo?moltid=GC19395&moltnbr=9993) expression is consistently higher in RCC cell lines, whereas that of MDM2 (experiment ID: 3080; https://dtp.cancer.gov/mtweb/targetinfo?moltid=GC12482&moltnbr=3080) expression is not. Expression of SQSTM1/P62 (experiment ID: 9233; https://dtp.cancer.gov/mtweb/targetinfo?moltid=GC18635&moltnbr=9233) is higher in most RCC cell lines. The graph is on a log scale (mRNA levels in cell line/mRNA levels in a reference pool). Reference probes were made by pooling equal amounts of mRNA from the HL-60, K562, NCI-H226, COLO205, SNB-19, LOX-IMVI, OVCAR-3, OVCAR-4, CAKI-1, PC-3, MCF7, and Hs578T cell lines. The average mRNA levels of TGM2, SQSTM1/P62, and MDM2 are 0.05, −0.05, and −0.09, respectively. (B) Kaplan–Meier survival curves based on expression of TGM2 or MDM2: Patients with high expressions of TGM 2 show shorter overall survival than those with low expression (p = 0.028). The overall survival of MDM2 is not significant (p = 0.21).
Fig 2: Transglutaminase 2 (TGase 2) and Mouse double minute 2 homolog (MDM2) destabilize p53 in renal cell carcinoma (RCC) under normoxic conditions. (A) ACHN (left) and CAKI-1 (right) cells were transfected for 24 h with siRNA targeting TGM2 or MDM2. Doxorubicin (1 µM) was used as a positive control. (B) Image J analysis of western blots in A. (C) Apoptosis assay to assess siTGM2 or siMDM2 silencing, as monitored by RealTime-Glo™ Annexin V under the same conditions as in A. Cumulative data from three independent experiments are shown (mean ± SD; n = 3). **p < 0.01 and ***p < 0.001.
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