Activation of JNK/p38 Pathway is Responsible for α-Methyl-n-butylshikonin Induced Mitochondria-Dependent Apoptosis in SW620 Human Colorectal Cancer Cells

Wang, Haibing; Ma, Xin

doi:10.7314/apjcp.2014.15.15.6321

Cited by 4 publications

(2 citation statements)

References 35 publications

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“…One powerful activity of this plant, apart from it containing essential nutrients required by humans, is to reduce the blood sugar level (Joseph and Jini 2013 ). Therefore, multiple investigations of proteins or metabolites in M. charantia were conducted, which demonstrated its hypoglycaemic effect, in addition to antitumor and antiviral activities, which have been well-documented worldwide (Fang and Ng 2011 ; Wang and Ma 2014 ). For example, momorcharins and Kuguacin J in M. charantia each possess a notable ability to inhibit human prostate cancer cells (Xiong et al.…”

Section: Discussionmentioning

confidence: 99%

Investigation of cell cytotoxic activity and molecular mechanism of 5β,19-epoxycucurbita-6,23( E )-diene-3β,19( R ),25-triol isolated from Momordica charantia on hepatoma cells

Yuan

Kao

et al. 2022

Pharmaceutical Biology

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Context Momordica charantia L. (Cucurbitaceae), known as bitter melon, is an edible fruit cultivated in the tropics. In this study, an active compound, 5β,19-epoxycucurbita-6,23( E )-diene-3β,19( R ),25-triol (ECDT), isolated from M. charantia was investigated in regard to its cytotoxic effect on human hepatocellular carcinoma (HCC) cells. Objective To examine the mechanisms of ECDT-induced apoptosis in HCC cells. Materials and methods The inhibitive activity of ECDT on HA22T HCC cells was examined by MTT assay, colony formation assay, wound healing assay, TUNEL/DAPI staining, annexin V-fluorescein isothiocyanate/propidium iodide (PI) staining and JC-1 dye. HA22T cells were treated with ECDT (5, 10, 15, 20 and 25 μM) for 24 h, and the molecular mechanism of cells apoptosis was examined by Western blot. Cells treated with vehicle DMSO were used as the negative control. Results ECDT inhibited the cell proliferation of HA22T cells in a dose-dependent manner. Flow cytometry showed that ECDT treatment at 10–20 μM increased early apoptosis by 10–14% and late apoptosis by 2–5%. Western blot revealed that ECDT treatment activated the mitochondrial-dependent apoptotic pathway, and ECDT-induced apoptosis was mediated by the caspase signalling pathway and activation of JNK and p38MAPK. Pre-treatment of cells with MAPK inhibitors (SB203580 or SP600125) reversed the ECDT-induced cell death, which further supported the involvement of the p38MAPK and JNK pathways. Discussion and conclusions Our results indicated that ECDT can induce apoptosis through the p38MAPK and JNK pathways in HA22T cells. The findings suggested that ECDT has a valuable anticancer property with the potential to be developed as a new chemotherapeutic agent for the treatment of HCC.

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Section: Discussionmentioning

confidence: 99%

Investigation of cell cytotoxic activity and molecular mechanism of 5β,19-epoxycucurbita-6,23( E )-diene-3β,19( R ),25-triol isolated from Momordica charantia on hepatoma cells

Yuan

Kao

et al. 2022

Pharmaceutical Biology

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“…Among the members of the MAPK family, c-Jun N-terminal protein kinase (JNK) is believed to regulate proapoptotic pathways and lead to cell death [56]. Conversely, the blockade of JNK may cause the resistance of cancer cells towards chemotherapy.…”

Section: Discussionmentioning

confidence: 99%

An Acetamide Derivative as a Camptothecin Sensitizer for Human Non‐Small‐Cell Lung Cancer Cells through Increased Oxidative Stress and JNK Activation

Chou

Fong

Lin

et al. 2016

Oxidative Medicine and Cellular Longevity

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In recent years, combination chemotherapy is a primary strategy for treating lung cancer; however, the issues of antagonism and side effects still limit its applications. The development of chemosensitizer aims to sensitize chemoresistant cancer cells to anticancer drugs and therefore improve the efficacy of chemotherapy. In this study, we examined whether N-[2-(morpholin-4-yl)phenyl]-2-{8-oxatricyclo[7.4.0.0,2,7]trideca-1(9),2(7),3,5,10,12-hexaen-4-yloxy}acetamide (NPOA), an acetamide derivative, sensitizes human non-small-cell lung cancer (NSCLC) H1299 cells towards camptothecin- (CPT-) induced apoptosis effects. Our results demonstrate that the combination of CPT and NPOA enhances anti-lung-cancer effect. The cytometer-based Annexin V/propidium iodide (PI) staining showed that CPT and NPOA cotreatment causes an increased population of apoptotic cells compared to CPT treatment alone. Moreover, Western blotting assay showed an enhancement of Bax expression and caspase cascade leading to cell death of H1299 cells. Besides, CPT and NPOA cotreatment-mediated disruption of mitochondrial membrane potential (MMP) in H1299 cells may function through increasing the activation of the stressed-associated c-Jun N-terminal kinase (JNK). These results showed that NPOA treatment sensitizes H1299 cells towards CPT-induced accumulation of cell cycle S phase and mitochondrial-mediated apoptosis through regulating endogenous ROS and JNK activation. Accordingly, NPOA could be a candidate chemosensitizer of CPT derivative agents such as irinotecan or topotecan in the future.

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Extracts derived from a traditional Chinese herbal formula triggers necroptosis in ectocervical Ect1/E6E7 cells through activation of RIP1 kinase

Chen

Liu

et al. 2019

Journal of Ethnopharmacology

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Activation of JNK/p38 Pathway is Responsible for α-Methyl-n-butylshikonin Induced Mitochondria-Dependent Apoptosis in SW620 Human Colorectal Cancer Cells

Cited by 4 publications

References 35 publications

Investigation of cell cytotoxic activity and molecular mechanism of 5β,19-epoxycucurbita-6,23( E )-diene-3β,19( R ),25-triol isolated from Momordica charantia on hepatoma cells

Investigation of cell cytotoxic activity and molecular mechanism of 5β,19-epoxycucurbita-6,23( E )-diene-3β,19( R ),25-triol isolated from Momordica charantia on hepatoma cells

An Acetamide Derivative as a Camptothecin Sensitizer for Human Non‐Small‐Cell Lung Cancer Cells through Increased Oxidative Stress and JNK Activation

Extracts derived from a traditional Chinese herbal formula triggers necroptosis in ectocervical Ect1/E6E7 cells through activation of RIP1 kinase

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