Melittin induces human gastric cancer cell apoptosis<i>via</i>activation of mitochondrial pathway

Kong, Guimei; Wenhua, Tao; Diao, Yali; Fang, Penghua; Wang, Jijun; Bo, Ping; Qian, Feng

doi:10.3748/wjg.v22.i11.3186

Cited by 74 publications

(57 citation statements)

References 45 publications

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“…Overall the data suggested that MEL can synergize with TRAIL in the induction of HCC cell apoptosis by activating the TAK1-JNK/p38 pathway but inhibiting the IκBα kinase-NFκB pathway [57]. Another study tested the efficacy of MEL in gastric cancer and observed that the agent induces apoptosis in SGC-7901 cells [58]. The accumulated data suggested that MEL induces early apoptosis, induces ROS levels, and induced caspase-3 activity.…”

Section: Anticancer Effects Of Bv and Its-conjugatesmentioning

confidence: 99%

Melittin, a major peptide component of bee venom, and its conjugates in cancer therapy

et al. 2017

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Melittin (MEL), a major peptide component of bee venom, is an attractive candidate for cancer therapy. This agent has shown a variety of anti-cancer effects in preclinical cell culture and animal model systems. Despite a convincing efficacy data against variety of cancers, its applicability to humans has met with challenges due to several issues including its non-specific cytotoxicity, degradation and hemolytic activity. Several optimization approaches including utilization of nanoparticle based delivery of MEL have been utilized to circumvent the issues. Here, we summarize the current understanding of the anticancer effects of bee venom and MEL on different kinds of cancers. Further, we also present the available information for the possible mechanism of action of bee venom and/or MEL.

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Section: Anticancer Effects Of Bv and Its-conjugatesmentioning

confidence: 99%

Melittin, a major peptide component of bee venom, and its conjugates in cancer therapy

et al. 2017

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“…Melittin has been proposed as a promising agent for anticancer therapy. Reportedly, MEL is prominently involved in the regulation of multifarious cancers, exemplified by hepatocellular carcinoma, breast cancer, lung cancer, leukaemia, ovarian carcinoma, gastric carcinoma, and prostate cancer . A handful of mechanisms of MEL cytotoxicity have been highlighted in various types of cancer cells (ie cell cycle alterations, effect on proliferation and/or inhibition of growth, induction of apoptosis.)…”

Section: Introductionmentioning

confidence: 99%

Melittin inhibits proliferation, migration and invasion of bladder cancer cells by regulating key genes based on bioinformatics and experimental assays

Yao

Zhang

et al. 2019

J Cellular Molecular Medi

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The antitumour effect of melittin (MEL) has recently attracted considerable attention. Nonetheless, information regarding the functional role of MEL in bladder cancer (BC) is currently limited. Herein, we investigated the effect of MEL on critical module genes identified in BC. In total, 2015 and 4679 differentially expressed genes (DEGs) associated with BC were identified from the GSE31189 set and The Cancer Genome Atlas database, respectively. GSE‐identified DEGs were mapped and analysed using Gene Ontology and Kyoto Encyclopaedia of Genes and Genomes analyses to determine BC‐involved crucial genes and signal pathways. Coupled with protein–protein interaction network and Molecular Complex Detection analyses, Modules 2 and 4 were highlighted in the progression of BC. In in‐vitro experiments, MEL inhibited the proliferation, migration, and invasion of UM‐UC‐3 and 5637 cells. The expression of NRAS, PAK2, EGFR and PAK1 in Module 4—enriched in the MAPK signalling pathway—was significantly reduced after treatment with MEL at concentrations of 4 or 6 μg/mL. Finally, quantitative reverse transcription‐polymerase chain reaction and Western blotting analyses revealed MEL inhibited the expression of genes at the mRNA (ERK1/2, ERK5, JNK and MEK5), protein (ERK5, MEK5, JNK and ERK1/2) and phosphorylation (p‐ERK1/2, p‐JNK, and p‐38) levels. This novel evidence indicates MEL exerts effects on the ERK5‐MAK pathway—a branch of MAPK signalling pathway. Collectively, these findings provide a theoretical basis for MEL application in BC treatment.

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“…The intrinsic apoptosis pathway is also called mitochondrial pathway or cytochrome c mediated pathway. Many studies have demonstrated that mitochondria play important roles in cell apoptosis [33,34]. Although there is no obvious morphological change for mitochondria, some channels on mitochondrial membranes are open during the process of cell apoptosis.…”

Section: Discussionmentioning

confidence: 99%

A farnesyl transferase inhibitor induces apoptosis of insulinoma pancreatic β cells of mouse

Gao¹,

Fu²,

Liu³

et al. 2018

biomedicalresearch

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This study is to investigate the effect of a Farnesyl Transferase Inhibitor (FTI) R115777 on apoptosis of mouse insulinoma pancreatic β cells. MTT assay was used to investigate the proliferative inhibition of in vitro cultured mouse insulinoma pancreatic β cell lines by a FTI R115777. The morphological changes of the cells were observed using a fluorescence microscope by staining with Hoechst 33258 and propidium iodide after the treatment with FTI R115777. The apoptosis rate of R115777-treated beta-TC-6 cells was detected by flow cytometry. The expressions of caspase-3 and caspase-9 of the R115777-treated beta-TC-6 cells were assayed by spectrophotometry. In addition, the sub-cellular distribution of cytochrome c and the expressions of Bax and Bcl-2 proteins were detected by Western blot. After the treatment with FTI R115777, the proliferation of the mouse insulinoma pancreatic β cell lines was significantly inhibited. Significant apoptosis was observed in the treated beta-TC-6 cells. The effect of R115777 on the apoptosis of beta-TC-6 cells showed time-and dose-dependent manners. The expressions of caspase-3, caspase-9 and Bax in the R115777-treated beta-TC-6 cells increased, while the expression of Bcl-2 decreased. The sub-cellular distribution of cytochrome-c changed, with reduced cytochrome-c in mitochondria and increased cytochrome-c in cytoplasm. FTI R115777 can inhibit the proliferation of mouse insulinoma pancreatic β cell lines, and might induce cell apoptosis through the mitochondrionmediated pathway. R115777 could be further studied as a potential antitumor drug.

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Melittin induces human gastric cancer cell apoptosisviaactivation of mitochondrial pathway

Abstract: Melittin can induce apoptosis of human gastric cancer (GC) cells through the mitochondria pathways, and it may be a potent agent in the treatment of human GC.

Cited by 74 publications

References 45 publications

Melittin, a major peptide component of bee venom, and its conjugates in cancer therapy

Melittin, a major peptide component of bee venom, and its conjugates in cancer therapy

Melittin inhibits proliferation, migration and invasion of bladder cancer cells by regulating key genes based on bioinformatics and experimental assays

A farnesyl transferase inhibitor induces apoptosis of insulinoma pancreatic β cells of mouse

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