First report on the isolation of melittin from Iranian honey bee venom and evaluation of its toxicity on gastric cancer AGS cells

Mahmoodzadeh, Amir; Zarrinnahad, Hannaneh; Bagheri, Kamran Pooshang; Moradia, Ali; Shahbazzadeh, Delavar

doi:10.1016/j.jcma.2015.06.008

Cited by 37 publications

(33 citation statements)

References 33 publications

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“…MEL was observed to induce necrosis in these cells as determined by morphological evaluation, DNA fragmentation assay, and flow cytometric analysis [66]. Similar observations were made in HCC N1S1, BEL-740261 and McA-RH7777 cells where MEL increased calpain activity and cell necrosis.…”

Section: Anticancer Effects Of Bv and Its-conjugatesmentioning

confidence: 55%

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: 55%

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

et al. 2017

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“…Since ATP generation in cancer cells is primarily from glycolysis as opposed to oxidative phosphorylation, even under normoxic conditions [38], the observed effect implies that glycolysis may be a potential target for melittin as an anticancer agent. The strong dependence of cancer cells on glycolysis could be the basis for melittin’s selective toxicity against them [13,14,15,16,17,18,19]. On the other hand, levels of ATP in A2780CR cells were higher than in A2780 at the outset and were not greatly affected by melittin treatment.…”

Section: Discussionmentioning

confidence: 99%

“…It has also been shown to have diverse anticancer effects in several different cancer cell lines including those of gastric [14,15], breast [12,16], ovarian [16,17], liver [18,19], prostate [16], cervical [16], and lung [20] origins. The mechanisms by which melittin, an amphipathic haemolytic peptide, exerts its potential anticancer effects include inhibition of cell proliferation [12,17], induction of apoptosis [12,14,15,21], and direct necrosis [14,15]. The mechanism of apoptosis appears to be related to the activation of the caspase-dependent pathway [15,16,21].…”

Section: Introductionmentioning

confidence: 99%

“…The mechanisms by which melittin, an amphipathic haemolytic peptide, exerts its potential anticancer effects include inhibition of cell proliferation [12,17], induction of apoptosis [12,14,15,21], and direct necrosis [14,15]. The mechanism of apoptosis appears to be related to the activation of the caspase-dependent pathway [15,16,21]. On the other hand, necrosis arises from damage to the cell membranes through necrotic cytotoxicity, as has been observed in rat thymocytes, murine skeletal muscle cells, gastrointestinal (GI) tumour cells, erythrocytes, lymphocytes, lymphoblastoid cells, rat primary alveolar cells, and intestinal Caco-2 cells [15,21].…”

Section: Introductionmentioning

confidence: 99%

“…The mechanism of apoptosis appears to be related to the activation of the caspase-dependent pathway [15,16,21]. On the other hand, necrosis arises from damage to the cell membranes through necrotic cytotoxicity, as has been observed in rat thymocytes, murine skeletal muscle cells, gastrointestinal (GI) tumour cells, erythrocytes, lymphocytes, lymphoblastoid cells, rat primary alveolar cells, and intestinal Caco-2 cells [15,21]. Melittin can also cause cell cycle arrest leading to inhibition of cell proliferation and growth.…”

Section: Introductionmentioning

confidence: 99%

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Metabolomic Profiling of the Effects of Melittin on Cisplatin Resistant and Cisplatin Sensitive Ovarian Cancer Cells Using Mass Spectrometry and Biolog Microarray Technology

et al. 2016

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In the present study, liquid chromatography-mass spectrometry (LC-MS) was employed to characterise the metabolic profiles of two human ovarian cancer cell lines A2780 (cisplatin-sensitive) and A2780CR (cisplatin-resistant) in response to their exposure to melittin, a cytotoxic peptide from bee venom. In addition, the metabolomics data were supported by application of Biolog microarray technology to examine the utilisation of carbon sources by the two cell lines. Data extraction with MZmine 2.14 and database searching were applied to provide metabolite lists. Principal component analysis (PCA) gave clear separation between the cisplatin-sensitive and resistant strains and their respective controls. The cisplatin-resistant cells were slightly more sensitive to melittin than the sensitive cells with IC50 values of 4.5 and 6.8 μg/mL respectively, although the latter cell line exhibited the greatest metabolic perturbation upon treatment. The changes induced by melittin in the cisplatin-sensitive cells led mostly to reduced levels of amino acids in the proline/glutamine/arginine pathway, as well as to decreased levels of carnitines, polyamines, adenosine triphosphate (ATP) and nicotinamide adenine dinucleotide (NAD+). The effects on energy metabolism were supported by the data from the Biolog assays. The lipid compositions of the two cell lines were quite different with the A2780 cells having higher levels of several ether lipids than the A2780CR cells. Melittin also had some effect on the lipid composition of the cells. Overall, this study suggests that melittin might have some potential as an adjuvant therapy in cancer treatment.

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Melittin: a possible regulator of cancer proliferation in preclinical cell culture and animal models

Haque,

Hussain,

Joshi

et al. 2023

J Cancer Res Clin Oncol

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First report on the isolation of melittin from Iranian honey bee venom and evaluation of its toxicity on gastric cancer AGS cells

Abstract: The present study indicated that melittin has an anticancer effect on gastric cancer AGS cells and stimulates necrotic cell death in these cells.

Cited by 37 publications

References 33 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

Metabolomic Profiling of the Effects of Melittin on Cisplatin Resistant and Cisplatin Sensitive Ovarian Cancer Cells Using Mass Spectrometry and Biolog Microarray Technology

Melittin: a possible regulator of cancer proliferation in preclinical cell culture and animal models

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