The effects of radiotherapy and concurrent chemoradiotherapy on cell proliferation, apoptosis and cell cycle of cervical squamous carcinoma
- Author:
Yan-Rong HAO
1
Author Information
1. Department of Radiation Oncology
- Publication Type:Journal Article
- Keywords:
Apoptosis;
Cell cycle;
Combined modality therapy;
Concurrent chemoradiotherapy;
Uterine cervical neoplasms
- From:
Tumor
2007;27(8):642-645
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To clarify the molecular mechanism underlying the response of locally advanced cervical squamous carcinoma to radiotherapy or concurrent chemoradiotherapy. Methods: Forty-nine patients were divided in to two groups. The 25 patients in radiotherapy (RT) group were given radiotherapy alone. The 24 patients in the concurrent chemoradiotherapy (CCRT) group were given 3 cycles of chemotherapy (DDP + 5-FU) in addition with RT. The specimens of the cervical tumors were obtained by biopsy before and during the treatment (10 Gy irradiation for RT group and 10 Gy irradiation plus one cycle of DDP + 5-FU chemotherapy for CCRT group). The cell cycle distribution was analyzed by flow cytometry (FCM). The apoptosis and PCNA expression in both groups were detected by TUNEL and immunohistochemical methods. Results: Apoptosis index (AI) and the positive rate of apoptosis were significantly increased after initiating RT and CCRT, respectively (P < 0.05, P < 0.001). There were also marked reduction of PCNA after 1 week of RT and CCRT (P = 0. 000 and P = 0.000). The CCRT significantly increased the apoptosis rate and decreased PCNA expression than RT (P = 0.03 and P = 0.005). Most cervical cancer cells were arrested in G2/M phase during RT treatment. However, CCRT induced S and G2/M phase arrest in a majority of cervical carcinoma cells. Conclusions: The additive or synergistic effects between chemotherapy and radiotherapy may be the mechanism for the effect of CCRT on locally advanced cervical squamous carcinoma CCRT induces apoptosis of tumor cells by inhibiting cell proliferation, inducing S and G2/M phase arrest, and synchronizing cell cycle.
