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Key regulators in bee venom-induced apoptosis are Bcl-2 and caspase-3 in human leukemic U937 cells through downregulation of ERK and Akt.
Int Immunopharmacol 2006; 6(12):1796-807II

Abstract

Bee venom (BV) has been known to inhibit proliferation and induce apoptosis in cancer cells. However, the molecular mechanisms involved in BV-induced apoptosis are still uncharacterized in human leukemic cells. In the present study, we report that BV induces apoptosis in leukemic U937 cells through downregulation of ERK and Akt signal pathway. Furthermore, BV-induced apoptosis was accompanied by downregulation of Bcl-2, activation of caspase-3 and a subsequent poly(ADP-ribose)polymerase (PARP) cleavages. The induction of apoptosis also was accompanied by the downregulation of the inhibitor of apoptosis protein (IAP) family proteins. Caspase-3 inhibitor, z-DEVD-fmk, was significantly capable of restoring cell viability and BV-induced apoptosis through caspase-3 activation was significantly attenuated in Bcl-2-overexpressing cells. These results indicate that downregulation of Bcl-2 plays a major role in the initiation as an activator of a caspase-3 involved with BV-induced apoptosis. BV also triggered the activation of p38 MAPK and JNK, and downregulation of ERK and Akt. PD98059 (an inhibitor of ERK) or LY294002 (an inhibitor of Akt), but not an inhibitor of p38 MAPK and JNK, significantly decreased cell viability and increased lactate dehydrogenase (LDH) release. The results indicated that key regulators in BV-induced apoptosis are Bcl-2 and caspase-3 in human leukemic U937 cells through downregulation of the ERK and Akt signal pathway.

Authors+Show Affiliations

Faculty of Applied Marine Science, Cheju National University, Jeju, South Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17052670

Citation

Moon, Dong-Oh, et al. "Key Regulators in Bee Venom-induced Apoptosis Are Bcl-2 and Caspase-3 in Human Leukemic U937 Cells Through Downregulation of ERK and Akt." International Immunopharmacology, vol. 6, no. 12, 2006, pp. 1796-807.
Moon DO, Park SY, Heo MS, et al. Key regulators in bee venom-induced apoptosis are Bcl-2 and caspase-3 in human leukemic U937 cells through downregulation of ERK and Akt. Int Immunopharmacol. 2006;6(12):1796-807.
Moon, D. O., Park, S. Y., Heo, M. S., Kim, K. C., Park, C., Ko, W. S., ... Kim, G. Y. (2006). Key regulators in bee venom-induced apoptosis are Bcl-2 and caspase-3 in human leukemic U937 cells through downregulation of ERK and Akt. International Immunopharmacology, 6(12), pp. 1796-807.
Moon DO, et al. Key Regulators in Bee Venom-induced Apoptosis Are Bcl-2 and Caspase-3 in Human Leukemic U937 Cells Through Downregulation of ERK and Akt. Int Immunopharmacol. 2006 Dec 5;6(12):1796-807. PubMed PMID: 17052670.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Key regulators in bee venom-induced apoptosis are Bcl-2 and caspase-3 in human leukemic U937 cells through downregulation of ERK and Akt. AU - Moon,Dong-Oh, AU - Park,Sung-Yong, AU - Heo,Moon-Soo, AU - Kim,Ki-Cheon, AU - Park,Cheol, AU - Ko,Woo Shin, AU - Choi,Yung Hyun, AU - Kim,Gi-Young, Y1 - 2006/08/22/ PY - 2006/06/27/received PY - 2006/07/21/revised PY - 2006/07/25/accepted PY - 2006/10/21/pubmed PY - 2007/1/11/medline PY - 2006/10/21/entrez SP - 1796 EP - 807 JF - International immunopharmacology JO - Int. Immunopharmacol. VL - 6 IS - 12 N2 - Bee venom (BV) has been known to inhibit proliferation and induce apoptosis in cancer cells. However, the molecular mechanisms involved in BV-induced apoptosis are still uncharacterized in human leukemic cells. In the present study, we report that BV induces apoptosis in leukemic U937 cells through downregulation of ERK and Akt signal pathway. Furthermore, BV-induced apoptosis was accompanied by downregulation of Bcl-2, activation of caspase-3 and a subsequent poly(ADP-ribose)polymerase (PARP) cleavages. The induction of apoptosis also was accompanied by the downregulation of the inhibitor of apoptosis protein (IAP) family proteins. Caspase-3 inhibitor, z-DEVD-fmk, was significantly capable of restoring cell viability and BV-induced apoptosis through caspase-3 activation was significantly attenuated in Bcl-2-overexpressing cells. These results indicate that downregulation of Bcl-2 plays a major role in the initiation as an activator of a caspase-3 involved with BV-induced apoptosis. BV also triggered the activation of p38 MAPK and JNK, and downregulation of ERK and Akt. PD98059 (an inhibitor of ERK) or LY294002 (an inhibitor of Akt), but not an inhibitor of p38 MAPK and JNK, significantly decreased cell viability and increased lactate dehydrogenase (LDH) release. The results indicated that key regulators in BV-induced apoptosis are Bcl-2 and caspase-3 in human leukemic U937 cells through downregulation of the ERK and Akt signal pathway. SN - 1567-5769 UR - https://www.unboundmedicine.com/medline/citation/17052670/Key_regulators_in_bee_venom_induced_apoptosis_are_Bcl_2_and_caspase_3_in_human_leukemic_U937_cells_through_downregulation_of_ERK_and_Akt_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1567-5769(06)00230-X DB - PRIME DP - Unbound Medicine ER -