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[Anticancer agents and apoptosis]
Abstract:
We reviewed recent investigations on apoptosis related to anticancer chemotherapy. The study of programmed cell death, apoptosis, has become one of the main stream in cellular biology, particularly in immunology, developmental biology and oncology. To determine whether the apoptotic cell death induced by anticancer agents could be inhibited by bcl-2 oncogene, we established a bcl-2 transfected human small cell lung cancer cell line, SBC-3/Bcl-2. SBC-3/Bcl-2 showed higher resistance to ADM, CPT-11 and MMC compared to the parental line SBC-3. Agarose gel electrophoresis showed typical DNA fragmentation of SBC-3 following treatment with CPT-11 or MMC. In contrast, the same concentration of the drugs did not induce DNA fragmentation in SBC-3/Bcl-2. However, there was no difference in sensitivity to CDDP, VP-16, ACNU, MTX and Taxol between SBC-3 and SBC-3/Bcl-2 (Ohmori T, et al: Biochem Biophys Res Commun 1993). These results suggest that bcl-2 can modulate the cytotoxicity of some anticancer agents by inhibiting the process of apoptosis. We speculate that some apoptotic pathways are bcl-2-dependent and others bcl-2-independent.
Insights
The bcl-2 oncogene inhibits apoptosis, making cancer cells resistant to certain chemotherapy drugs like CPT-11 and MMC. This suggests bcl-2 impacts specific cancer cell death pathways.
Area of Science:
- Oncology
- Cellular Biology
- Immunology
Context:
- Apoptosis, or programmed cell death, is crucial in oncology, immunology, and developmental biology.
- Anticancer chemotherapy effectiveness can be influenced by programmed cell death mechanisms.
- The role of the bcl-2 oncogene in modulating chemotherapy-induced apoptosis requires further investigation.
Purpose:
- To investigate if the bcl-2 oncogene can inhibit chemotherapy-induced apoptosis.
- To determine the impact of bcl-2 expression on the sensitivity of small cell lung cancer cells to various anticancer agents.
Summary:
- A bcl-2 transfected human small cell lung cancer cell line (SBC-3/Bcl-2) was established and compared to the parental line (SBC-3).
- SBC-3/Bcl-2 exhibited increased resistance to ADM, CPT-11, and MMC, with reduced DNA fragmentation compared to SBC-3.
- No significant difference in sensitivity was observed for CDDP, VP-16, ACNU, MTX, and Taxol, indicating bcl-2-dependent and independent apoptotic pathways.
Impact:
- Results suggest bcl-2 can modulate the cytotoxicity of specific anticancer drugs by inhibiting apoptosis.
- This finding implies that some apoptotic pathways are regulated by bcl-2, while others are not.
- Understanding these pathways could inform the development of more effective cancer therapies.