Zhao Pengjun, Jiang Hao, Su Dan, Feng Jianguo, Ma Shenglin, Zhu Xinhai
Department of Radiation Oncology, Hangzhou Cancer Hospital, Hangzhou, Zhejiang 310002, P.R. China.
Department of Oncology, Zhejiang Hospital, Hangzhou, Zhejiang 310013, P.R. China.
Mol Med Rep. 2015 Jan;11(1):327-32. doi: 10.3892/mmr.2014.2655. Epub 2014 Oct 15.
Rhizoma paridis is widely used for cancer therapy due to its potential involvement in the suppression of tumor growth. However, at present there is no clear explanation for the mechanism underlying the inhibitory effects of Rhizoma paridis combined with hyperthermia on tumor growth. The aim of the present study was to evaluate the effects of Paris saponin I (PSI) combined with hyperthermia on a variety of non-small cell lung cancer (NSCLC) cell lines. An MTT assay was used to determine the levels of growth inhibition. The cell cycle was analyzed using flow cytometry and cell apoptosis was analyzed with Annexin V/propidium iodide staining and the Hoechst assay. The morphology of cells during apoptosis was determined using a transmission electron microscope. The expression levels of B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax) and caspase-3 proteins were detected using western blotting. The inhibition rates significantly increased with PSI in combination with hyperthermia at 43˚C. PSI with hyperthermia at 43˚C caused G2/M phase arrest and significantly induced apoptosis. The expression level of Bcl-2 decreased, while Bax expression increased following treatment with PSI with hyperthermia at 43˚C. In addition, the protein expression of caspase-3 was significantly enhanced. PSI combined with hyperthermia is a potent antitumor treatment through the inhibition of proliferation of NSCLC cells and may be developed as a new antitumor therapy. PSI combined with hyperthermia significantly induced apoptosis through a multi regulatory process involving G2/M arrest and regulation of Bax, Bcl-2 and caspase-3 expression, resulting in cell death and tumor inhibition.
重楼因其可能参与抑制肿瘤生长而被广泛用于癌症治疗。然而，目前对于重楼联合热疗抑制肿瘤生长的潜在机制尚无明确解释。本研究的目的是评估重楼皂苷I（PSI）联合热疗对多种非小细胞肺癌（NSCLC）细胞系的影响。采用MTT法测定生长抑制水平。使用流式细胞术分析细胞周期，并用膜联蛋白V/碘化丙啶染色和Hoechst检测法分析细胞凋亡。使用透射电子显微镜观察凋亡过程中细胞的形态。采用蛋白质印迹法检测B细胞淋巴瘤2（Bcl-2）、Bcl-2相关X蛋白（Bax）和半胱天冬酶-3蛋白的表达水平。PSI联合43˚C热疗时抑制率显著增加。PSI联合43˚C热疗导致G2/M期阻滞并显著诱导细胞凋亡。43˚C热疗联合PSI处理后，Bcl-2表达水平降低，而Bax表达增加。此外，半胱天冬酶-3的蛋白表达显著增强。PSI联合热疗通过抑制NSCLC细胞增殖是一种有效的抗肿瘤治疗方法，可能发展成为一种新的抗肿瘤疗法。PSI联合热疗通过涉及G2/M阻滞以及Bax、Bcl-2和半胱天冬酶-3表达调控的多调节过程显著诱导细胞凋亡，导致细胞死亡和肿瘤抑制。
