Apoptosis of Colorectal Cancer UTC116 Cells Induced by Cantharidinate

Liu, Bin; Gao, Huimin; Xu, Jianlin; Cao, Hong; Fang, Xuedong; Gao, Hai‐Mei; Qiao, Shubin

doi:10.7314/apjcp.2012.13.8.3705

Cited by 7 publications

(5 citation statements)

References 18 publications

(11 reference statements)

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“…A number of studies have reported that CTD exerted an inhibitory effect on cell proliferation by inducing apoptosis in a variety of tumor cells, including gastric, colorectal and pancreatic cancer cell lines (20)(21)(22). The results of the present study also demonstrated that CTD had a similar effect in promoting the apoptosis of NSCLC cells, by detecting levels of apoptotic markers, including anti-apoptosis protein Bcl-2 and pro-apoptosis proteins like Bax and active caspase-3.…”

Section: Discussionsupporting

confidence: 76%

Cantharidin suppresses cell growth and migration, and activates autophagy in human non-small cell lung cancer cells

Liu

et al. 2018

Oncol Lett

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Abstract. Cantharidin (CTD), a component of Mylabris (blister beetle), is a traditional Chinese medicine that exerts an anticancer effect in multiple types of cancer cells. The aim of the present study was to investigate whether CTD exhibited anti-metastatic and inhibitory cell proliferation effects against human non-small cell lung cancer (NSCLC) A549 cells, and the possible underlying mechanism by which this occurs. The results of the present study demonstrated that CTD arrested proliferation, suppressed invasion and migration and induced apoptosis in A549 cells in vitro. Alterations of apoptosis-associated protein levels, including B-cell lymphoma-2 (Bcl-2), Bcl-associated X (Bax) and active caspase-3, were detected. Furthermore, the present study demonstrated that CTD activated autophagy through downregulation of p62 expression and upregulation of microtubule-associated proteins 1A/1B light chain 3B and Beclin-1 expression. Additionally, western blot analysis identified that CTD inhibited the phosphatidylinositol 3-kinase (PI3K)/RAC serine/threonine protein kinase (Akt)/mechanistic target of rapamycin (mTOR) signaling pathway in NSCLC, demonstrating that the levels of phosphorylated (p-)Akt, p-mTOR, phosphorylated ribosomal p70S6 protein kinase (p-p70-S6K) and cyclin D1 were significantly decreased following treatment with CTD. In conclusion, the results of the present study indicated that CTD impeded cell growth and migration by inhibiting PI3K/Akt/mTOR signaling in NSCLC, and promoted autophagy and apoptosis. CTD exhibited anticancer activity against NSCLC in vitro, revealing it as a potential candidate for the treatment of NSCLC.

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Section: Discussionsupporting

confidence: 76%

Cantharidin suppresses cell growth and migration, and activates autophagy in human non-small cell lung cancer cells

Liu

et al. 2018

Oncol Lett

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“…Certain traditional Chinese medicines, including CTD, have been demonstrated to be reasonable and effective treatments for cancer. It has been reported that CTD has an effect on several types of human cancer, including pancreatic ( 12 ), bladder ( 13 ), hepatocellular ( 15 ) and colorectal ( 20 ) cancer. However, it remains unclear whether CTD is effective in treating gastric cancer as well.…”

Section: Discussionmentioning

confidence: 99%

Cantharidin induces G2/M phase arrest and apoptosis in human gastric cancer SGC-7901 and BGC-823 cells

et al. 2014

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The aim of the present study was to investigate the effect of cantharidin (CTD) on human gastric cancer cells and to explore the underlying mechanisms of these effects. The human gastric cancer SGC-7901 and BGC-823 cell lines were treated with CTD. MTS assays were then employed to examine cellular proliferation, flow cytometry was used to analyze the cell cycle and apoptosis, and western blot analysis was used to determine protein expression levels. It was found that CTD inhibited the proliferation of the human gastric cancer SGC-7901 and BGC-823 cells in a dose- and time-dependent manner in vitro. CTD also induced G2/M phase arrest and cellular apoptosis in a dose-dependent manner. In addition, CTD increased the levels of p21, caspase-7, -8 and -9, activated caspase-3, poly ADP ribose polymerase and Bad, but decreased the levels of cyclin-dependent kinase 1, cyclin A and B, B-cell lymphoma-2 (Bcl-2) and Bid. The present results suggested that CTD may inhibit the proliferation of human gastric cancer SGC-7901 and BGC-823 cells in vitro by inducing G2/M phase arrest and cell apoptosis. CTD may induce cellular G2/M phase arrest by regulating cycle-associated proteins and induce apoptosis by activating a caspase cascade or regulating the Bcl-2 family proteins.

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“…In addition, paclitaxel has been used for clinical treatment of breast cancer, ovarian cancer, and other tumors, oridonin has been used for the treatment of lung cancer, esophageal cancer, and liver cancer, and retinoic acid has shown efficacy in treatment of leukemia [ 26 – 28 ]. There have been numerous studies showing that CTD induces cell cycle arrest and apoptosis in a variety of human cancers, including pancreatic cancer [ 29 ], bladder cancer [ 16 ], colorectal cancer [ 30 ], and hepatocellular carcinoma [ 31 ].…”

Section: Discussionmentioning

confidence: 99%

Cantharidin Inhibits Anti-Apoptotic Bcl-2 Family Proteins and Induces Apoptosis in Human Osteosarcoma Cell Lines MG-63 and MNNG/HOS via Mitochondria-Dependent Pathway

et al. 2018

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BackgroundCantharidin (CTD) is one of the major active ingredients of blister beetles and has significant antitumor activity in many cancer cell lines. The aim of our study was to evaluate the effect of CTD on the apoptosis of human osteosarcoma cells MG-63 and MNNG/HOS, and to explore the possible molecular mechanism.Material/MethodsOsteosarcoma cells MG-63 and MNNG/HOS were treated with varying concentrations of CTD. The proliferation inhibition of cells was detected by MTS. Flow cytometry and Hoechst 33258 staining were used to determine cell cycle arrest and apoptosis, and apoptosis-related protein levels were analyzed by Western blotting.ResultsOur current findings suggest that CTD could inhibit the proliferation of these 2 osteosarcoma cells. The cells treated with CTD showed an obvious apoptotic morphology, and CTD promoted cells apoptosis in a dose-dependent manner. In addition, cantharidin-induced apoptosis was accompanied by increased expression of Bax and PARP and decreased expression of Bcl-2, p-Akt, and p-Cdc2.ConclusionsCTD accelerates the apoptosis of MG-63 and MNNG/HOS cells in a concentration-dependent manner through the mitochondria-dependent pathway, suggesting that use of CTD is a novel approach for the treatment of osteosarcoma.

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Apoptosis of Colorectal Cancer UTC116 Cells Induced by Cantharidinate

Cited by 7 publications

References 18 publications

Cantharidin suppresses cell growth and migration, and activates autophagy in human non-small cell lung cancer cells

Cantharidin suppresses cell growth and migration, and activates autophagy in human non-small cell lung cancer cells

Cantharidin induces G2/M phase arrest and apoptosis in human gastric cancer SGC-7901 and BGC-823 cells

Cantharidin Inhibits Anti-Apoptotic Bcl-2 Family Proteins and Induces Apoptosis in Human Osteosarcoma Cell Lines MG-63 and MNNG/HOS via Mitochondria-Dependent Pathway

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