Sann-Joong-Kuey-Jian-Tang decreases the protein expression of mammalian target of rapamycin but increases microtubule associated protein II light chain 3 expression to inhibit human BxPC‑3 pancreatic carcinoma cells

三重桂建汤降低哺乳动物雷帕霉素靶蛋白的表达,但增加微管相关蛋白 II 轻链 3 的表达,以抑制人类 BxPC‑3 胰腺癌细胞

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作者:Chin-Cheng Su

Abstract

Sann‑Joong‑Kuey‑Jian‑Tang (SJKJT), a Traditional Chinese Medicinal prescription, has been used for the treatment of lymphadenopathy and solid tumors, and has shown therapeutic potential in a number of human malignant tumor cell lines, such as Hep‑G2 hepatocellular carcinoma cells. Previous mechanistic studies demonstrated that SJKJT inhibited the proliferation of BxPC‑3 pancreatic carcinoma cells through the extrinsic and intrinsic apoptotic pathways in vitro. SJKJT was also shown to be cytotoxic to colo 205 colon cancer cells by inducing autophagy in vitro. The present study therefore investigated molecular mechanisms of autophagy in human BxPC‑3 pancreatic cancer cells treated with SJKJT. The cytotoxic effects of SJKJT on BxPC‑3 human pancreatic carcinoma cells were evaluated using an MTT assay. Furthermore, the expression of autophagy‑associated proteins, including mammalian target of rapamycin (mTOR), beclin‑1, autophagocytosis‑associated protein (Atg)3, Atg7, Atg5‑Atg12 and microtubule‑associated protein II light chain 3 (LC3‑II), was assessed using western blot analysis. The results demonstrated that BxPC‑3 cells treated with SJKJT exhibited decreased expression levels of mTOR and increased expression of LC3‑II protein. In addition, the expression of the beclin‑1, Atg3, Atg7 and Atg5‑Atg12 proteins was increased during the first 24 h, but decreased from 48 to 72 h. The results showed that SJKJT inhibited the proliferation of human BxPC‑3 pancreatic cancer cells in vitro. A possible underlying molecular mechanism may be the induction of autophagy. Further investigation into the therapeutic potential of SJKJT in human pancreatic cancer is required.

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