PLCε Can Promote Bladder Cancer Cell T24 Survival via GLS/p-mTOR Pathway
YUAN Hongling1, FAN Jiaxin1, YANG Jinxiao1, LI Ting1, HE Zhenting1, WU Xiaohou2, CHEN Qi3, OU Liping1*, LUO Chunli1*
Glutamine which is the most abundant amino acid in the blood, plays a particularly important role in cell growth and metabolism. One of the characteristics of tumor metabolism is glutamine addiction. This study investigated whether PLCε can regulate autophagy and promote the survival of bladder cancer cells T24 targeted by GLS (glutaminase). Firstly, PLCε expression in bladder cancer was analyzed using Su Multi-cancer Statistics, Sanchez-Carbayo Bladder 2 database and cell culture experiment. Results showed that PLCε highly expressed in bladder cancer. Then, shPLCε cell lines were established by transfecting LV-shPLCε into bladder cancer cell T24. The expression of PLCε in bladder cancer cell T24 and its effects on apoptosis and autophagy were detected by q-PCR and Western blot. Meanwhile, the changes of autophagy spot (LC3) were detected by immunofluorescence. The results illustrated that PLCε knockdown increased the expression of Caspase-3/Caspase-8/LC3-II, apoptosis cell ratio and decreased p62; meanwhile increased the number of green autophagy spots LC3 in the cytoplasm by immunofluorescence and inhibited the expression of GLS and p-mTOR. Adding GLS over-expression plasmid into shPLCε group decreased the expression of LC3-II and the number of LC3 autophagy spots, and improved p-mTOR/p62 expression. However the results were reversed after adding GLS knockdown plasmids. This study showed that PLCε could inhibit autophagy in bladder cancer cell T24 via GLS/p-mTOR, thus promoting the survival of tumor cells.
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