Effect of ginsenoside Rg3 on proliferation and apoptosis of 786-0 cells and AktmTORSTAT3 signaling in renal carcinoma

• Autor(a) principal: LI,Hongwei
• Data de Publicação: 2022
• Outros Autores: WANG,Tong, CUI,Wei, GAO,Zhan, CHE,Zi
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Food Science and Technology (Campinas)
• Texto Completo: http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0101-20612022000101031
• topic: ginsenoside Rg; kidney cancer 786-O cell; cell apoptosis; cell proliferation

Abstract Surgery is currently the major approach treating kidney cancer, which is insensitive to chemo-/radio-therapy. However, due to the limitation of current diagnostic technique, certain number of patients has lost the opportunity of surgery. Therefore the searching for novel effective treatment approach is of critical importance. Ginsenoside Rg3 can inhibit proliferation and induce apoptosis of various tumor cells. It effect in kidney cancer, however, is still lacked. This study thus treated kidney cancer cell line 786-O with ginsenoside Rg3 to illustrate its effect on cell proliferation and apoptosis, and investigated possible mechanism.Gradient concentrations of ginsenoside Rg3 was used to treat 786-O cells, whose proliferation was measured by CCK8 assay. The apoptotic rate was quantified using flow cytometry. Western blotting was used to measure protein expression levels of p-Akt, p-mTOR and p-STAT3. Ginsenoside Rg3 significantly inhibited proliferation of kidney cancer cell 786-O in a dose- and time-dependent manner: higher concentration and longer treatment time caused more significant inhibition on cell proliferation. Similar patterns also occurred for the induction for cell apoptosis by ginsenoside Rg3. The expression levels of p-Akt, p-mTOR and p-STAT3, however, were decreased with higher dosages of ginsenoside Rg3, and were negatively correlated with apoptotic ratio. Ginsenoside Rg3 can exert anti-tumor role via inducing apoptosis and inhibiting proliferation of 786-O cells, possibly via the blocking of Akt/mTOR/STAT3 pathway.