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481 DIFFERENTIAL SENSITIVITY OF HEAD AND NECK SQUAMOUS CELL CANCER CELL LINES TO CISPLATIN-MEDIATED CELL DEATH.
  1. S. Ahmed1,
  2. M. S. Veena2,
  3. C. G. Tang1,
  4. M. B. Wang2,3,
  5. E. S. Srivatsan2,3
  1. 1David Geffen School of Medicine at UCLA, Los Angeles, CA
  2. 2Department of Surgery, Veterans Affairs Greater Los Angeles Healthcare System, Los Angeles, CA
  3. 3Department of Surgery, University of California, Los Angeles, CA

Abstract

As the fifth most common cancer in the world, head and neck squamous cell carcinoma (HNSCC) continues to have a poor prognosis. One of the standard treatment options is a protocol that uses cisplatin-a platinum-based chemotherapy drug-along with radiation therapy. However, the molecular mechanism of cisplatin-mediated growth arrest is not fully understood. The goals of this study were to (1) compare the cisplatin sensitivity of two different HNSCC cell lines and (2) determine the appropriate conditions for conducting future experiments that decipher cisplatin's mechanism. The cell-killing effects of cisplatin were studied in vitro on CCL23 (laryngeal squamous cell carcinoma) and CAL27 (tongue squamous cell carcinoma). The cells were treated with cisplatin (6 μg/mL) for durations of 1, 4, 6, and 8 hours and then incubated in media for 0, 24, 48, and 72 hours. In CCL23 cells, there was greater than 50% cell death after 24 hours of incubation for the 4-, 6-, and 8-hour treatment durations. The maximum rate of cell death occurred at a treatment duration of 1 hour and incubation of 24 to 48 hours. In CAL27 cells, none of the treatment durations produced 50% cell death after 24 hours' incubation. The maximum rate of cell death occurred at a treatment duration of 6 hours and incubation duration of 24 to 48 hours. The data suggest that CCL23 is more sensitive to cisplatin than CAL27. The data also demonstrate the optimal conditions required to achieve measurable cell death in the two cell lines. These conditions are currently being used to conduct experiments that investigate the down-regulation of NF-κB activity through interactions with p16 and p21. We hope that identifying potential biological markers-such as p16-can provide diagnostic tools for cisplatin sensitivity and thus be helpful in the stratification of future patients for cisplatin treatment.

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