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CDDP induces p53-dependent apoptosis in tongue cancer cells

H Kanata1, K Yane, I Ota

  • 1Department of Otorhinolaryngology, NARA Medical University, Kashihara, Nara, Japan. jibika@nmu-gw.naramed-u.ac.jp

International Journal of Oncology
|August 12, 2000
PubMed

Insights

Wild-type p53 (SAS) tongue cancer cells showed higher cisplatin sensitivity and apoptosis than mutant-type p53 (HSC-4) cells. p53 status may predict response to cisplatin therapy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Cisplatin (CDDP) is a chemotherapy drug used to treat various cancers.
  • The p53 tumor suppressor gene plays a critical role in cell cycle regulation and apoptosis.
  • Understanding the role of p53 in chemoresistance is crucial for optimizing cancer treatment.

Purpose of the Study:

  • To investigate the differential sensitivity of tongue cancer cell lines with wild-type and mutant p53 to cisplatin.
  • To explore the correlation between p53 status, Bax protein expression, and apoptosis induction following cisplatin treatment.

Main Methods:

  • Western blot analysis to assess p53 and Bax protein levels.
  • Hoechst 33342 staining and electrophoresis to detect apoptosis.
  • Comparison of cisplatin sensitivity (D10 dose) in SAS (wild-type p53) and HSC-4 (mutant-type p53) cell lines.

Main Results:

  • SAS cells exhibited approximately 2-fold higher sensitivity to cisplatin compared to HSC-4 cells.
  • CDDP treatment increased p53 and Bax protein levels in SAS cells, correlating with observed apoptosis.
  • HSC-4 cells showed p53 overexpression without CDDP and no significant Bax elevation or apoptosis induction.

Conclusions:

  • Wild-type p53 status is associated with increased cisplatin sensitivity and apoptosis in tongue cancer cells.
  • p53 acts as a positive regulator of Bax expression, promoting apoptosis.
  • p53 genetic status may serve as a predictive biomarker for cisplatin therapy response in tongue cancer.

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