Sann-Joong-Kuey-Jian-Tang decreases the protein expression of Mcl-1 and TCTP and increases that of TNF-α and Bax in BxPC-3 pancreatic carcinoma cells
Sann-Joong-Kuey-Jian-Tang decreases the protein expression of Mcl-1 and TCTP and increases that of TNF-α and Bax in BxPC-3 pancreatic carcinoma cells
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DOI：
10.3892/ijmm.2013.1369
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发表时间：
2013-07-01
影响因子：
5.4
通讯作者：
Su, Chin-Cheng
中科院分区：
文献类型：
--
作者：
Chien, Su-Yu;Kuo, Shou-Jen;Su, Chin-Cheng
三重归健汤（Sann-Joong-Kuey-Jian-Tang，SJKJT）是一种传统的中药方剂，已被用于治疗淋巴结病和实体瘤，并在几种人类恶性肿瘤细胞系中显示出治疗潜力。然而，SJKJT在人胰腺癌中的疗效和分子作用机制尚未阐明。本研究采用MTT法检测了四肾康煎剂对人胰腺癌细胞BxPC-3的细胞毒作用。Western blot检测BxPC-3细胞中髓细胞白血病1蛋白（Mcl-1）、免疫控制肿瘤蛋白（TCTP）、肿瘤坏死因子-α（TNF-α）、caspase-8、caspase-3、Bax和Bcl-2家族的蛋白表达水平。流式细胞仪分析细胞周期。免疫细胞化学（ICC）法检测caspase-3蛋白表达。结果表明，SJKJT抑制BxPC-3细胞的增殖，并呈时间和剂量依赖性。SJKJT处理后BxPC-3细胞TNF-α、caspase-8、caspase-3和Bax蛋白表达水平升高，Mcl-1、TCTP和Bcl-xL蛋白表达水平降低。结果还表明，SJKJT增加BxPC-3细胞在亚G1期的百分比。ICC染色结果显示，经SJKJT处理的BxPC-3细胞caspase-3蛋白表达上调。这些结果表明，SJKJT抑制BxPC-3细胞的增殖通过外源性和内源性途径，在体外诱导凋亡。我们的研究，使用BxPC-3人胰腺癌细胞，表明SJKJT有潜力作为胰腺癌治疗的化疗药物。进一步的研究是必要的，充分阐明其作用机制。
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 several human malignant tumor cell lines. However, the efficacy and molecular mechanisms of action of SJKJT in human pancreatic cancer have not yet been elucidated. In the present study, we evaluated the cytotoxic effects of SJKJT on BxPC-3 human pancreatic carcinoma cells by MTT assay. The protein expression levels of myeloid cell leukemia 1 protein (Mcl-1), translationally controlled tumor protein (TCTP), tumor necrosis factor-a (TNF-alpha), caspase-8, caspase-3, Bax and Bcl-2 family in the BxPC-3 cells were measured by western blot analysis. The cell cycle was analyzed by flow cytometry. The protein expression of caspase-3 was also detected by immunocytochemistry (ICC). The results revealed that SJKJT inhibited the proliferation of BxPC-3 cells in a time- and dose-dependent manner. The protein expression levels of TNF-a, caspase-8, caspase-3 and Bax increased in the BxPC-3 cells treated with SJKJT; however, the levels of Mcl-1, TCTP and Bcl-xL decreased. The results also demonstrated that SJKJT increased the percentage of BxPC-3 cells in the sub-G1 phase. In addition, ICC staining indicated that the protein expression of caspase-3 was upregulated in the BxPC-3 cells treated with SJKJT. These findings indicate that SJKJT inhibits the proliferation of BxPC-3 cells through the extrinsic and intrinsic pathway, inducing apoptosis in vitro. Our study, using BxPC-3 human pancreatic cancer cells, demonstrates that SJKJT has potential as a chemotherapeutic agent for the treatment of pancreatic cancer. Further sutdies are warranted to fully elucidate its mechanisms of action.