Bee Venom Enhanced Cytotoxic Effect of Natural Killer Cells on Human Lung Cancer Through Inducing Extrinsic Apoptosis
- Authors
- Jung Hyun Kim; 송호섭
- Issue Date
- 2014
- Publisher
- 대한침구의학회
- Keywords
- Bee venom; Lung cancer; A549; NCI-H460; NK-92; Death receptor; Nitric oxide(NO)
- Citation
- Journal of Acupuncture Research, v.31, no.1, pp.111 - 119
- Journal Title
- Journal of Acupuncture Research
- Volume
- 31
- Number
- 1
- Start Page
- 111
- End Page
- 119
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/13967
- ISSN
- 2586-288X
- Abstract
- Objectives : I investigated whether Bee Venom can synergistically strengthen the cytotoxic effects of NK-92 cells, enhancing the inhibition of the growth of Lung Cancer Cells including A549 and NCI-H460 through induction of death receptor dependent extrinsic apoptosis and NO generation in the Nitro-oxide pathway.
Methods : Bee Venom inhibited cell proliferation of A549 or NCI-H460 Human Lung Cancer Cells as well as NK-92 Cells. Moreover, when they were co-punctured with NK cells and concomitantly treated by 3 ㎍/㎖ of Bee Venom, more influence was exerted on inhibition of proliferation of A549 or NCI-H460 Human Lung Cancer Cells than BV or NK cell co-culture alone.
Results : The expression of Fas, TNFR2, DR3, DR6 in A549 Lung Cancer Cells was significantly increased by co-culture of NK-92 cells and treatment of 3 ㎍/㎖ of Bee Venom, compared to co-culture of NK-92 cells alone, whereas the expression of Fas, TNFR2, DR6 in NCI-H460 Lung Cancer Cells was significantly increased by co-culture of NK-92 cells, representing no synergistic effects in the co-culture of NK-92 cell and concomitant treatment of 3 ㎍/㎖ of Bee Venom. Coincidently, caspase-8, a expression of pro-apoptotic proteins in the extrinsic apoptosis pathway demonstrated same results as the above. Meanwhile, In NO generation, there is little change of NO generation in co-culture of NK-92 cells with A549 cells as well as the co-culture of NK-92 cell with them and concomitant treatment of 3 ㎍/㎖ of Bee Venom, whereas increase of NO generation was shown in co-culture of NK-92 cells with NCI-H460 cells as well as the co-culture of NK-92 cell with them and concomitant treatment of 3 ㎍/㎖ of Bee Venom, although synergistic effects by Bee Venom was not found.
Conclusions : These present data provide that Bee Venom could be useful candidate compounds to enhance lung cancer growth inhibiting ability of NK-92 cells through DR expression and the related apoptosis.
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