Radiosensitization of p53-Deficient Lung Cancer Cells by Pre-treatment with Cytostatic Compounds

• Published in: Anticancer research Vol. 32; no. 4; pp. 1239 - 1243
• Main Authors: TOKALOV, Sergey V, ABOLMAALI, Nasreddin
• Format: Journal Article
• Language: English
• Published: Attiki International Institute of Anticancer Research 01.04.2012
• Subjects: Antineoplastic Agents - pharmacology; Biological and medical sciences; Cell Line, Tumor; Cisplatin; Cisplatin - pharmacology; Cytotoxicity; Doxorubicin; Doxorubicin - pharmacology; Flow Cytometry; Humans; Ionizing radiation; Lung cancer; Lung Neoplasms - metabolism; Lung Neoplasms - pathology; Medical sciences; Mitosis; p53 protein; Paclitaxel; Pneumology; Radiation Tolerance - drug effects; Radiosensitivity; Radiosensitization; Radiotherapy; Synchronization; Tumor Suppressor Protein p53 - metabolism; Tumors; Tumors of the respiratory system and mediastinum; Lung disease; Flow cytometry; Respiratory disease; Cytostatic; Lung cancer; A549; Radiation; Malignant tumor; FaDu; p53; Chemotherapy; Treatment; Cancerology; TP53 Gene; Radiosensitization; H1299 cell lines; Cell cycle; Established cell line; Bronchus disease; Tumor cell; Cancer; Tumor suppressor gene
• ISSN: 0250-7005; 1791-7530

This study specifies a strategy to improve radiotherapy by partial synchronization of p53-deficient cancer cells (FaDu and H1299) in mitosis using taxol, with protecting p53 wild-type cells (A549) by the prior administration of cytostatic compounds. Cytotoxic and cytostatic effects of ionizing radiation, cisplatin, doxorubicin and taxol, administrated alone or in combination were investigated in vitro by flow cytometry. A protective effect of doxorubicin but not cisplatin was found after administration of triple sequence with ionizing radiation and taxol. It was found that preliminary administration of doxorubicin induced growth arrest and protected A549 cells from the taxol/radiation treatment, while simultaneously killing FaDu and H1299 cells. The proposed therapeutic strategy allows protection of p53 wild-type cells and selectively increases radiosensitivity of p53-deficient cancer cells.