Cofilin-1 overexpression and its role in tumor growth and progression in systemic malignancies

Kapoor, Shailendra

doi:10.3109/09553002.2013.825065

Cited by 5 publications

(7 citation statements)

References 7 publications

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“…Cofilin 1 is expressed in most embryonic and adult mammalian cells, Cofilin 2 is expressed in muscle cells, and ADF is restricted to epithelia and endothelia [ 9 ]. Cofilin 1, the non-muscle isoform of the cofilin 1 gene product, plays a key role in cell migration and cytokinesis and is directly associated with the invasion, metastasis, and chemoresistance of various human malignant solid tumors [ 11 , 15 , 16 , 17 ]. Protein kinase D1 (PKD 1) enhances phosphorylation and de-phosphorylates Cofilin 1 to maintain it in its inactive form [ 18 , 19 ].…”

Section: Introductionmentioning

confidence: 99%

Cofilin 1 promotes bladder cancer and is regulated by TCF7L2

Wang

et al. 2017

Oncotarget

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Earlier reports demonstrated that Cofilin expression is increased in bladder cancer samples, though its function remains unknown. Here, we found that Cofilin 1 expression was higher in bladder cancer tissues than in paracancerous tissues. Overexpression of Cofilin 1 promoted, while Cofilin 1 knockdown inhibited, proliferation, migration, and invasion in the T24 and RT4 bladder cancer cell lines. In addition, Cofilin 1 overexpression increased, while Cofilin 1 knockdown decreased, bladder tumor volumes in mouse xenograft experiments. Transcription factor 7-like 2 (TCF7L2) targeted the promoter of the Cofilin 1 gene, and TCF7L2 knockdown or mutations in the Cofilin 1 promoter dramatically decreased Cofilin 1 transcription. TCF7L2 promoted cell proliferation and migration and increased Cofilin 1 protein levels in RT4 and T24 cells. Thus, TCF7L2 contributed to Cofilin 1-induced promotion of bladder cancer development by binding to the Cofilin 1 promoter and increasing its expression.

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Section: Introductionmentioning

confidence: 99%

Cofilin 1 promotes bladder cancer and is regulated by TCF7L2

Wang

et al. 2017

Oncotarget

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“…The high expression of cofilin-1 in malignant cells can enhance the speed of cell migration, while silencing cofilin-1 can delay cancer cell metastasis (15). Cofilin-1 can depolymerize actin filaments by binding directly to actin and make the actin filaments turn over quickly (23,24), thus controlling cell movement, which serves an important role in the proliferation and migration of tumor cells (11). Cofilin 1 is involved in tumor invasion, metastasis and prognosis by regulating actin reorganization and pseudopodia formation; sustained activation of cofilin 1 promotes the formation and migration of filamentous pseudopodia in prostate cancer cells and enhances the metastatic ability of prostate cancer in vivo (25).…”

Section: Discussionmentioning

confidence: 99%

“…A basic function of cofilin is to combine with and depolymerize F-actin intracellularly, thereby inhibiting G-actin polymerization and accelerating actin filament dynamic transformation (10). At the same time, cofilin plays an important role in regulating cell movement (11). The cofilin 1 pathway is regarded as a target to suppress the growth of breast cancer cells (12) and also serves an important role in inhibiting epithelial mesenchymal transition in gastric adenocarcinoma cells (13).…”

Section: Diallyl Disulfide Induces Downregulation and Inactivation Ofmentioning

confidence: 99%

Diallyl disulfide induces downregulation and inactivation of cofilin�1 differentiation via the Rac1/ROCK1/LIMK1 pathway in leukemia cells

Ling

Lei

et al. 2020

Int J Oncol

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Cofilin is associated with cell differentiation; however, to the best of our knowledge, no data have indicated an association between the cofilin 1 pathway and leukemia cell differentiation. The present study investigated the involvement of the cofilin 1 signaling pathway in diallyl disulfide (DADS)-induced differentiation and the inhibitory effects on the proliferation, migration, and invasion of human leukemia HL-60 cells. First, it was identified that 8 µM DADS suppressed cell proliferation, migration and invasion, and induced differentiation based on the reduced nitroblue tetrazolium ability and increased CD11b and CD33 expression. DADS significantly downregulated the expression of cofilin 1 and phosphorylated cofilin 1 in HL-60 leukemia cells. Second, it was verified that silencing cofilin 1 markedly promoted 8 µM DADS-induced differentiation and the inhibitory effect on cell proliferation and invasion. Overexpression of cofilin 1 obviously suppressed 8 µM DADS-induced differentiation and the inhibitory effect on cell proliferation and invasion. Third, the present study examined the mechanisms by which 8 µM DADS decreases cofilin 1 expression and activation. The results revealed that 8 µM DADS inhibited the mRNA and protein expression of Rac1, Rho-associated protein kinase 1 (ROCK1) and LIM domain kinase 1 (LIMK1) as well as the phosphorylation of LIMK1 in HL-60 cells, while 8 µM DADS enhanced the effects of the Rac1-ROCK1-LIMK1 pathway in cells overexpressing cofilin 1 compared with that in control HL-60 cells. These results suggest that the anticancer function of DADS on HL-60 leukemia cells is regulated by the Rac1-ROCK1-LIMK1-cofilin 1 pathway, indicating that DADS could be a promising anti-leukemia therapeutic compound.

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“…Cofilin and its regulatory proteins mediate specific signaling pathways that can change actin conformation, promote cytoskeleton reorganization, induce invasive pseudopod formation, and participate in the invasion and metastasis of malignant tumors . Phosphorylated cofilin is inactive, whereas its activated form is nonphosphorylated.…”

Section: Discussionmentioning

confidence: 99%

Tissue microarray analysis reveals that cofilin expression is a poor prognostic factor in juvenile nasopharyngeal angiofibroma

Wang

et al. 2019

Int Forum Allergy Rhinol

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Background: Juvenile nasopharyngeal angiofibroma (JNA) has a high recurrence rate a er surgery. Cofilin overexpression is associated with increased tumor cell metastasis, and progression of various human cancers. However, studies on cofilin expression in JNA are rare. The purpose of this study was to investigate the expression and localization of cofilin in a tissue microarray (TMA) of JNA specimens. In addition, we also analyzed its correlation with clinicopathological features and recurrence. Methods:Immunohistochemistry was performed to detect cofilin expression in a TMA of samples from 70 JNA patients and 10 control subjects. The association between clinicopathological variables and cofilin immunostaining was analyzed using Pearson's chi-square test. Kaplan-Meier survival analysis was used to calculate the disease-free survival rate, and investigate the effect of cofilin expression on time to recurrence (TTR) in JNA patients. The Cox regression model was used for multivariate survival analysis. Results:Cofilin was detected in irregular smooth muscle cells, pericytes, less differentiated stromal cells, and plump cells, but not in inactive fibroblasts and mature vascular endothelial cells of JNA specimens. The presence of cofilin in JNA was correlated with tumor stage (p = 0.012) and volume of intraoperative hemorrhage (p < 0.001). JNA patients with high cofilin expression had a higher recurrence rate than those with low cofilin expression (p = 0.012). Cofilin expression and patient's age were significant predictors of TTR, and cofilin was a be er predictor for disease recurrence (area under the receiver operating curve [AU-ROC; 0.711; p = 0.005) than other clinicopathological features. Conclusion:Cofilin is an independent prognostic marker for JNA patients who have undergone surgical treatment and may represent a novel therapeutic target for extensive JNA. C 2019 ARS-AAOA, LLC.

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Cofilin-1 overexpression and its role in tumor growth and progression in systemic malignancies

Cited by 5 publications

References 7 publications

Cofilin 1 promotes bladder cancer and is regulated by TCF7L2

Cofilin 1 promotes bladder cancer and is regulated by TCF7L2

Diallyl disulfide induces downregulation and inactivation of cofilin�1 differentiation via the Rac1/ROCK1/LIMK1 pathway in leukemia cells

Tissue microarray analysis reveals that cofilin expression is a poor prognostic factor in juvenile nasopharyngeal angiofibroma

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