Study on Cellular Localization of Bin Toxin and its Apoptosis-inducing Effect on Human Nasopharyngeal Carcinoma Cells
Issued Date
2023-01-01
Resource Type
ISSN
15680096
eISSN
18735576
Scopus ID
2-s2.0-85150311549
Pubmed ID
36424771
Journal Title
Current Cancer Drug Targets
Volume
23
Issue
5
Start Page
388
End Page
399
Rights Holder(s)
SCOPUS
Bibliographic Citation
Current Cancer Drug Targets Vol.23 No.5 (2023) , 388-399
Suggested Citation
Kanwal S., Boonserm P. Study on Cellular Localization of Bin Toxin and its Apoptosis-inducing Effect on Human Nasopharyngeal Carcinoma Cells. Current Cancer Drug Targets Vol.23 No.5 (2023) , 388-399. 399. doi:10.2174/1568009623666221124102524 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/82225
Title
Study on Cellular Localization of Bin Toxin and its Apoptosis-inducing Effect on Human Nasopharyngeal Carcinoma Cells
Author(s)
Author's Affiliation
Other Contributor(s)
Abstract
Background: Bacterial pore-forming toxins, BinA and BinB together known as the binary toxin are potent insecticidal proteins, that share structural homology with antitumor bacterial parasporin-2 protein. The underlying molecular mechanism of Bin toxin-induced cancer cell cytotox-icity requires more knowledge to understand whether the toxin induced human cytotoxic effects oc-cur in the same way as that of parasporin-2 or not. Methods: In this study, anticancer properties of Lysinibacillus sphaericus derived Bin toxin on HK1 were evaluated through MTT assay, morphological analysis and lactate dehydrogenase efflux assay. Induction of apoptosis was determined from RT-qPCR, caspase activity and cytochrome c release as-say. Internalization pattern of Bin toxin in HK1 cells was studied by confocal laser-scanning micro-scopic analysis. Results: Activated Bin toxin had strong cytocidal activity to HK1 cancer cell line at 24 h post-inoculation. Both BinA and BinB treated HK1 cells showed significant inhibition of cell viability at 12 µM. Induction of apoptotic mediators from RT-qPCR and caspase activity analyses indicated the activation of programmed cell death in HK1 cells in response to Bin toxin treatment. Internalization pattern of Bin toxin studied by using confocal microscopy indicated the localization of BinA on cell surface and internalization of BinB in the cytoplasm of cancer cells as well as colocalization of BinA with BinB. Evaluation of cytochrome c release also showed the association of BinB and BinA+BinB with mitochondria. Conclusion: Bin toxin is a cytotoxic protein that induces cytotoxic and apoptotic events in HK1 cells, and may have high therapeutic potential as an anti-cancer agent.