Euphorbia factor L2 induces apoptosis in A549 cells through the mitochondrial pathway

Lin, Min-Ting; Tang, Sili; Zhang, Chao; Chen, Hubiao; Huang, Wenjing; Liu, Yun; Zhang, Jianye

doi:10.1016/j.apsb.2016.06.008

Cited by 52 publications

(46 citation statements)

References 23 publications

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“…To the best of our knowledge, apoptosis can be induced by two alternative signaling pathways: The death receptor pathway and the mitochondrial pathway. The action of many anticancer drugs is mediated through the mitochondrial pathway (18,(22)(23)(24). Additionally, many reports show that cinobufagin is effective in the prevention and treatment of cancer by triggering apoptosis and autophagic cell death via activation of the ROS/JNK/p38 axis (8).…”

Section: Discussionmentioning

confidence: 99%

“…This effect was reversed in the HBSC group. Once the mitochondrial programmed cell death pathway is activated, the mitochondrial permeability transition pore opens and membrane potential decreases (23,24). JC-1 dye is used to monitor mitochondrial membrane potential and exhibits enhanced green fluorescence when membrane potential is disrupted.…”

Section: Discussionmentioning

confidence: 99%

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Inhibition of autophagy enhances cinobufagin‑induced apoptosis in gastric cancer

et al. 2018

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Cinobufagin is a cardiotoxic bufanolide steroid secreted by the Asiatic toad Bufo gargarizans. Cinobufagin is one of the active ingredients in the anticancer Chinese medicine called Chan Su, which was demonstrated to be an effective treatment for gastric cancer. Increasing evidence shows that inhibition of autophagy has a pro-apoptotic effect on human gastric cancer cells. The aim of the present study was to investigate the relationship between cinobufagin, autophagy and apoptosis in gastric cancer. Autophagy was induced or inhibited in the human gastric cancer cell line SGC-7901 by incubation in HBSS media or by treatment with 3-methyladenine or ATG5 siRNA, respectively. Following treatment, the levels of apoptosis, apoptotic proteins, reactive oxygen species (ROS), and mitochondrial membrane potential were compared between the conditions. As anticipated, we found that cinobufagin increased apoptosis in SGC-7901 cells. Notably, inhibition of autophagy, monitored by the absence of the autophagosome marker LC3-II, also enhanced cell apoptosis. This effect was reversed when autophagy was induced by incubation in HBSS media. Enhanced expression of pro-apoptotic indicators, including BAX, cytosolic cytochrome c, cleaved PARP, caspase-3 and caspase-9, was detected when autophagy was suppressed. Increased pro-apoptotic protein expression was accompanied by disrupted mitochondrial membrane potential and elevated ROS production. Altogether, these data suggest that inhibition of autophagy enhances the anticancer action of cinobufagin through increased apoptosis of gastric cancer cells. Moreover, these effects may be partly mediated by ROS generation and the activation of the mitochondrial programmed cell death pathway.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Inhibition of autophagy enhances cinobufagin‑induced apoptosis in gastric cancer

et al. 2018

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“…The half maximal inhibitory concentration (IC 50 ) value was used to determine the growth-inhibitory effect of costunolide, which was calculated from the concentration-response curve using the Bliss method (SPSS version 16.0; SPSS, Inc.). Cell survival was calculated using a formula as previously described (3). medium, containing 10% FBS was added to the lower chamber, which acted as a chemoattractant.…”

Section: Methodsmentioning

confidence: 99%

“…Plants have long been considered a rich source of bioactive natural products, some of which exhibit potent activity as potential anticancer agents (3)(4)(5)(6)(7). Costunolide is a sesquiterpene lactone (Fig.…”

Section: Introductionmentioning

confidence: 99%

Costunolide induces apoptosis and inhibits migration and invasion in H1299 lung cancer cells

Wei

Qiu

et al. 2020

Oncol Rep

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Costunolide being a sesquiterpene lactone, is known to have anticancer properties. The present study investigated the anticancer effects of costunolide against the H1299 human non-small-cell lung cancer (NSCLC) cell line. Inhibition of cell viability by costunolide was assessed via a MTT assay. Furthermore, the apoptotic rate was detected using Annexin V/propidium iodide labeling. A colony forming cell assay was performed to investigate the antiproliferative effects of costunolide. Wound healing and Transwell assays were performed to determine the inhibitory effects of costunolide on migration and invasion, respectively. Western blot analysis was undertaken to determine protein expression, and reverse transcription-quantitative PCR was performed to assess mRNA expression levels. The results demonstrated that costunolide inhibited the viability of H1299 cells, with a half maximal inhibitory concentration value of 23.93±1.67 µM and induced cellular apoptosis in a dose-dependent manner. Furthermore, the colony formation, migrative and invasive abilities of the H1299 cells were inhibited in a dose-or time-dependent manner. The protein expression levels of E-cadherin increased and those of N-cadherin decreased following treatment with costunolide, which suggested that costunolide inhibited epithelial-to-mesenchymal transition. The mRNA levels of B-Raf, E-cadherin, N-cadherin, integrins α2 and β1, as well as matrix metalloproteinases 2 were also found to be regulated costunolide. These findings indicate the potential of costunolide in the treatment of NSCLC.

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“…The mitochondrial pathway has been relatively well researched and is controlled predominantly by members of caspase-3, cleaved caspase-3, and B-cell lymphoma 2 (Bcl-2) and Bcl-2-associated X protein. Certain natural products, including Euphorbia factor L2 and bruceine D, can induce cell apoptosis through the mitochondrial pathway (35,36). Cell apoptosis can be induced by miR-133b and miR-135a in vitro via a signaling cascade, involving JAK2, STAT3 and Bcl-2 (37).…”

Section: Discussionmentioning

confidence: 99%

miRNA‑135a regulates Hut78 cell proliferation via the GATA‑3/TOX signaling pathway

Wei

Liu

Guo³

et al. 2019

Mol Med Report

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The present study investigated the role of microRNA-135a (miR-135a) in cutaneous T-cell lymphoma (CTCL) proliferation. Compared with the normal T lymphocyte control cell line, the mRNA and protein levels of GATA binding protein 3 (GATA-3) were markedly increased in the Hut78 cell line and miR-135a was markedly decreased (P<0.05). Based on bioinformatics, the target gene of miR-135a was identified as GATA-3. Dual luciferase and pre-miR-135a assays showed that miR-135a regulated the translation of GATA-3. In addition, the overexpression of miR-135a mimics decreased the protein levels of GATA-3 and thymocyte selection-associated high mobility group box (TOX). The substantially increased mRNA and protein levels of GATA-3 may be associated with the downregulation of miR-135a, leading to T-cell deregulation and proliferation through GATA-3/TOX regulation and subsequently causing CTCL.

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Euphorbia factor L2 induces apoptosis in A549 cells through the mitochondrial pathway

Cited by 52 publications

References 23 publications

Inhibition of autophagy enhances cinobufagin‑induced apoptosis in gastric cancer

Inhibition of autophagy enhances cinobufagin‑induced apoptosis in gastric cancer

Costunolide induces apoptosis and inhibits migration and invasion in H1299 lung cancer cells

miRNA‑135a regulates Hut78 cell proliferation via the GATA‑3/TOX signaling pathway

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