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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2024.12
- 수록면
- 276 - 283 (8page)
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Objectives: This study investigates the effects of amifostine on cell proliferation and apoptosis in HCT116 colorectal cancer cells, with a specific focus on the roles of p53 and c-Abl proteins.
Methods: IC50 values were determined across various cell lines to assess drug sensitivity. The sensitivity of c-Abl+/+ and c-Abl–/– cells to amifostine was compared to evaluate the influence of c-Abl on drug response. Cell cycle progression was analyzed by assessing G2/M checkpoint arrest induced by amifostine. DNA damage was quantified by measuring r-H2AX accumulation. Apoptosis rates were determined, and the expression balance between Bcl-2 and Bax was analyzed to investigate their role in regulating cell survival and death.
Results: c-Abl+/+ cells exhibited higher sensitivity to amifostine than c-Abl–/– cells. Interestingly, p53-deficient cell lines showed increased sensitivity to amifostine. Amifostine treatment induced G2/M checkpoint arrest, thereby inhibiting cell cycle progression in HCT116 cells. A significant accumulation of r-H2AX, a marker of DNA damage, was observed, with p53-deficient cells displaying higher levels of DNA damage. The presence of p53 significantly influenced apoptosis rates ( P = 0.002), and the balance between Bcl-2 and Bax expression was critical in determining cell survival and death.
Conclusion: Amifostine inhibits the proliferation of colorectal cancer cells through p53 signaling pathways. The study provides valuable insights into the role of p53 and c-Abl proteins in modulating the response to amifostine, suggesting that targeting these pathways could offer therapeutic potential for the treatment of colorectal cancer.
Methods: IC50 values were determined across various cell lines to assess drug sensitivity. The sensitivity of c-Abl+/+ and c-Abl–/– cells to amifostine was compared to evaluate the influence of c-Abl on drug response. Cell cycle progression was analyzed by assessing G2/M checkpoint arrest induced by amifostine. DNA damage was quantified by measuring r-H2AX accumulation. Apoptosis rates were determined, and the expression balance between Bcl-2 and Bax was analyzed to investigate their role in regulating cell survival and death.
Results: c-Abl+/+ cells exhibited higher sensitivity to amifostine than c-Abl–/– cells. Interestingly, p53-deficient cell lines showed increased sensitivity to amifostine. Amifostine treatment induced G2/M checkpoint arrest, thereby inhibiting cell cycle progression in HCT116 cells. A significant accumulation of r-H2AX, a marker of DNA damage, was observed, with p53-deficient cells displaying higher levels of DNA damage. The presence of p53 significantly influenced apoptosis rates ( P = 0.002), and the balance between Bcl-2 and Bax expression was critical in determining cell survival and death.
Conclusion: Amifostine inhibits the proliferation of colorectal cancer cells through p53 signaling pathways. The study provides valuable insights into the role of p53 and c-Abl proteins in modulating the response to amifostine, suggesting that targeting these pathways could offer therapeutic potential for the treatment of colorectal cancer.
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