International Journal of Radiation Biology, January 2014; 90(1): 113 © 2014 Informa UK, Ltd. ISSN 0955-3002 print / ISSN 1362-3095 online DOI: 10.3109/09553002.2013.825065
Cofilin-1 overexpression and its role in tumor growth and progression in systemic malignancies Shailendra Kapoor
Int J Radiat Biol Downloaded from informahealthcare.com by The University of Manchester on 01/14/15 For personal use only.
Private Practice, Mechanicsville, VA, USA
Sir : I read with great interest the recent article by Leu et al. (2013) concerning the role of cofilin-1 in cell radiosensitivity. It is interesting to note that cofilin-1 may also play a major role in tumor growth and progression in a number of systemic malignancies. For instance, cofilin-1 plays a major role in tumor progression in ovarian carcinomas. In fact, nearly 64% of all ovarian tumors are positive for cofilin-1 (Zhou et al. 2012). The ‘progression-free survival’ rates in patients with cofilin1-positive tumors are markedly reduced in comparison to the ‘progression-free survival’ rates in those with cofilin1-negative ovarian malignancies (Li et al. 2013). Similarly, a close relationship has been established between chemoresistance to taxols and phosphorylated cofilin-1 levels (Nishimura et al. 2011). Up-regulation of phosphorylated cofilin-1 results in increased chemoresistance. These changes have been shown both in vivo and in vitro. A similar relationship is seen in bladder carcinomas. Tumor invasiveness in bladder carcinomas is markedly augmented following cofilin-1 phosphorylation within the tumor cells (Chung et al. 2013). Typically, cofilin-1 phosphorylation is markedly increased by EGF (Endothelial growth factor). Similar results are seen in prostatic malignancies. In fact, agents such as 23,24-dihydrocucurbitacin F attenuate tumor growth in prostate carcinomas by inducing the formation of cofilin-actin rods within the cancerous cells (Ren et al. 2012). Similarly, knockdown of cofilin-1 results in increased sensitivity of prostate carcinomas to chemotherapeutic agents such as docetaxel (Pérez-Martinez et al. 2012).
The above examples clearly illustrate the significant role of cofilin-1 in tumor pathogenesis and the need for further studies in this regard.
Declaration of interest The author report no conflicts of interest. The author alone is responsible for the content and writing of the paper.
References Chung H, Kim B, Jung SH, et al. 2013. Does phosphorylation of cofilin affect the progression of human bladder cancer? BMC Cancer 13:45. Leu JD, Chiu YW, Lo CC , et al. 2013. Enhanced cellular radiosensitivity induced by cofilin-1 over-expression is associated with reduced DNA repair capacity. International Journal of Radiation Biology 89:433–444. Li M, Yin J, Mao N, Pan L. 2013. Upregulation of phosphorylated cofilin 1 correlates with taxol resistance in human ovarian cancer in vitro and in vivo. Oncology Reports 29:58–66. Nishimura S, Tsuda H, Kataoka F, et al. 2011. Overexpression of cofilin 1 can predict progression-free survival in patients with epithelial ovarian cancer receiving standard therapy. Human Pathology 42:516–521. Pérez-Martinez FC, Carrión B, Lucio MI, et al. 2012. Enhanced docetaxel-mediated cytotoxicity in human prostate cancer cells through knockdown of cofilin-1 by carbon nanohorn delivered siRNA . Biomaterials 33:8152–8159. Ren S, Ouyang DY, Saltis M, et al. 2012. Anti-proliferative effect of 23,24dihydrocucurbitacin F on human prostate cancer cells through induction of actin aggregation and cofilin-actin rod formation. Cancer Chemotherapy and Pharmacology 70:415–424. Zhou J, Wang Y, Fei J, Zhang W. 2012. Expression of cofilin 1 is positively correlated with the differentiation of human epithelial ovarian cancer. Oncology Letters 4:1187–1190.
Correspondence: Dr Shailendra Kapoor, Private practice, Mechanicsville, VA, USA. E-mail: [email protected] (Received 14 May 2013; revised 25 June 2013; accepted 4 July 2013)
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Cofilin-1 overexpression and its role in tumor growth and progression in systemic malignancies Shailendra Kapoor
Int J Radiat Biol Downloaded from informahealthcare.com by The University of Manchester on 01/14/15 For personal use only.
Private Practice, Mechanicsville, VA, USA
Sir : I read with great interest the recent article by Leu et al. (2013) concerning the role of cofilin-1 in cell radiosensitivity. It is interesting to note that cofilin-1 may also play a major role in tumor growth and progression in a number of systemic malignancies. For instance, cofilin-1 plays a major role in tumor progression in ovarian carcinomas. In fact, nearly 64% of all ovarian tumors are positive for cofilin-1 (Zhou et al. 2012). The ‘progression-free survival’ rates in patients with cofilin1-positive tumors are markedly reduced in comparison to the ‘progression-free survival’ rates in those with cofilin1-negative ovarian malignancies (Li et al. 2013). Similarly, a close relationship has been established between chemoresistance to taxols and phosphorylated cofilin-1 levels (Nishimura et al. 2011). Up-regulation of phosphorylated cofilin-1 results in increased chemoresistance. These changes have been shown both in vivo and in vitro. A similar relationship is seen in bladder carcinomas. Tumor invasiveness in bladder carcinomas is markedly augmented following cofilin-1 phosphorylation within the tumor cells (Chung et al. 2013). Typically, cofilin-1 phosphorylation is markedly increased by EGF (Endothelial growth factor). Similar results are seen in prostatic malignancies. In fact, agents such as 23,24-dihydrocucurbitacin F attenuate tumor growth in prostate carcinomas by inducing the formation of cofilin-actin rods within the cancerous cells (Ren et al. 2012). Similarly, knockdown of cofilin-1 results in increased sensitivity of prostate carcinomas to chemotherapeutic agents such as docetaxel (Pérez-Martinez et al. 2012).
The above examples clearly illustrate the significant role of cofilin-1 in tumor pathogenesis and the need for further studies in this regard.
Declaration of interest The author report no conflicts of interest. The author alone is responsible for the content and writing of the paper.
References Chung H, Kim B, Jung SH, et al. 2013. Does phosphorylation of cofilin affect the progression of human bladder cancer? BMC Cancer 13:45. Leu JD, Chiu YW, Lo CC , et al. 2013. Enhanced cellular radiosensitivity induced by cofilin-1 over-expression is associated with reduced DNA repair capacity. International Journal of Radiation Biology 89:433–444. Li M, Yin J, Mao N, Pan L. 2013. Upregulation of phosphorylated cofilin 1 correlates with taxol resistance in human ovarian cancer in vitro and in vivo. Oncology Reports 29:58–66. Nishimura S, Tsuda H, Kataoka F, et al. 2011. Overexpression of cofilin 1 can predict progression-free survival in patients with epithelial ovarian cancer receiving standard therapy. Human Pathology 42:516–521. Pérez-Martinez FC, Carrión B, Lucio MI, et al. 2012. Enhanced docetaxel-mediated cytotoxicity in human prostate cancer cells through knockdown of cofilin-1 by carbon nanohorn delivered siRNA . Biomaterials 33:8152–8159. Ren S, Ouyang DY, Saltis M, et al. 2012. Anti-proliferative effect of 23,24dihydrocucurbitacin F on human prostate cancer cells through induction of actin aggregation and cofilin-actin rod formation. Cancer Chemotherapy and Pharmacology 70:415–424. Zhou J, Wang Y, Fei J, Zhang W. 2012. Expression of cofilin 1 is positively correlated with the differentiation of human epithelial ovarian cancer. Oncology Letters 4:1187–1190.
Correspondence: Dr Shailendra Kapoor, Private practice, Mechanicsville, VA, USA. E-mail: [email protected] (Received 14 May 2013; revised 25 June 2013; accepted 4 July 2013)
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