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Updated: May 26, 2026

An Orthotopic Bladder Cancer Model for Gene Delivery Studies
Published on: December 1, 2013
Bee venom induces apoptosis through intracellular Ca2+ -modulated intrinsic death pathway in human bladder cancer
Siu-Wan Ip1, Yung-Lin Chu, Chun-Shu Yu
1Department of Nutrition, China Medical, Taipei, Taiwan.
Objectives:
To focus on bee venom-induced apoptosis in human bladder cancer TSGH-8301 cells and to investigate its signaling pathway to ascertain whether intracellular calcium iron (Ca(2+)) is involved in this effect.
Methods:
Bee venom-induced cytotoxic effects, productions of reactive oxygen species and Ca(2+) and the level of mitochondrial membrane potential (ΔΨm) were analyzed by flow cytometry. Apoptosis-associated proteins were examined by Western blot analysis and confocal laser microscopy.
Results:
Bee venom-induced cell morphological changes and decreased cell viability through the induction of apoptosis in TSGH-8301 cell were found. Bee venom promoted the protein levels of Bax, caspase-9, caspase-3 and endonuclease G. The enhancements of endoplasmic reticulum stress-related protein levels were shown in bee venom-provoked apoptosis of TSGH-8301 cells. Bee venom promoted the activities of caspase-3, caspase-8, and caspase-9, increased Ca(2+) release and decreased the level of ΔΨm. Co-localization of immunofluorescence analysis showed the releases of endonuclease G and apoptosis-inducing factor trafficking to nuclei for bee venom-mediated apoptosis. The images revealed evidence of nuclear condensation and formation of apoptotic bodies by 4',6-diamidino-2-phenylindole staining and DNA gel electrophoresis showed the DNA fragmentation in TSGH-8301 cells.
Conclusions:
Bee venom treatment induces both caspase-dependent and caspase-independent apoptotic death through intracellular Ca(2+) -modulated intrinsic death pathway in TSGH-8301 cells.
Insights
Bee venom induces apoptosis in human bladder cancer cells by affecting cell viability and promoting key proteins. Intracellular calcium plays a role in this cell death pathway.
Area of Science:
- Oncology
- Biochemistry
- Cell Biology
Background:
- Human bladder cancer (TSGH-8301 cells) is a significant health concern.
- Apoptosis is a critical process in cancer therapy.
Purpose of the Study:
- Investigate bee venom's effect on apoptosis in human bladder cancer cells.
- Elucidate the signaling pathway involved, focusing on intracellular calcium (Ca(2+)).
Main Methods:
- Flow cytometry to analyze cytotoxic effects, reactive oxygen species, Ca(2+) levels, and mitochondrial membrane potential (ΔΨm).
- Western blot and confocal microscopy to examine apoptosis-associated proteins.
- Nuclear staining (4',6-diamidino-2-phenylindole) and DNA gel electrophoresis to assess apoptosis hallmarks.
Main Results:
- Bee venom decreased cell viability and induced apoptosis in TSGH-8301 cells.
- Increased levels of apoptosis-related proteins (Bax, caspases, endonuclease G) and endoplasmic reticulum stress markers.
- Bee venom elevated Ca(2+) release, decreased ΔΨm, and triggered nuclear condensation and DNA fragmentation.
Conclusions:
- Bee venom induces both caspase-dependent and -independent apoptosis in bladder cancer cells.
- Intracellular Ca(2+) modulates the intrinsic death pathway, contributing to bee venom-mediated apoptosis.
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