Radiotherapy is the major treatment modality for uterine cervical cancer, but in some cases, the disease is radioresistant. Defining the molecular events that contribute to radioresistance and progression of cancer are of critical importance. Here we evaluated the role of Fused Toes Homolog (FTS) in radiation resistance of cervical carcinoma. Immunostaning of cervical cancer cells and tissues revealed that FTS localization and expression was changed after radiation. Targeted stable knockdown of FTS in HeLa cells led to the growth inhibition after radiation. Radiation induced AKT mediated cytoprotective effect was countered by FTS knockdown which leads to PARP cleavage and caspase-3 activation leading to cell death. FTS knockdown promotes radiation induced cell cycle arrest at G0/G1 and apoptosis of HeLa cells with concurrent alterations in the display of cell cycle regulatory proteins. This study revealed FTS is involved in radioresistance of cervical cancer. Targeted inhibition of FTS led to the shutdown of key elemental characteristics of cervical cancer and could lead to an effective therapeutic strategy.
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Acknowledgments The authors would like to thank Mrs. Jeong-Seon Jeon for her excellent technical assistance. This research was supported by the program of Basic Atomic Energy Research Institute (BAERI), which is a part of the Nuclear R & D Programs funded by the Ministry of Education, Science and Technology (MEST) of Korea in 2009.
- Cell cycle
- Cervical cancer
- Fused Toes Homolog