Study on the Significance of Cofilin 1 Overexpression in Human Bladder Cancer

Wang, Fei; Wu, Dinglan; He, Feifei; Fu, Housheng; Xu, Jianbing; Chen, Jianxiang; Zhang, Shufang; Wang, Weifu

doi:10.5301/tj.5000569

Cited by 8 publications

(14 citation statements)

References 18 publications

(19 reference statements)

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“…In this study, we found that Cofilin 1 expression was higher in bladder cancer tissues than in paracancerous tissues, which is consistent with previous results [ 32 ]. We also examined the effects of Cofilin 1 in the T24 and RT4 bladder cancer cell lines.…”

Section: Discussionsupporting

confidence: 93%

“…Cofilin 1 also promoted bladder cancer growth in mouse xenograft experiments. Together, these results and previous studies suggest that Cofilin 1 may be a therapeutic target for bladder cancer [ 8 , 32 ]. ChIP and luciferase assays demonstrated that the transcription factor TCF7L2 bound to the promoter region of Cofilin 1 to regulate its expression.…”

Section: Discussionsupporting

confidence: 82%

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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: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 82%

Cofilin 1 promotes bladder cancer and is regulated by TCF7L2

Wang

et al. 2017

Oncotarget

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“…Cofilin overexpression has been seen in lung cancer cells undergoing EMT [ 48 ] and in association with increased tumor cell invasion or metastasis [ 34 , 49 – 51 ]. Collazo and coworkers reported augmented levels of active cofilin in human prostate cancer and in experimental prostate tumors [ 33 ].…”

Section: Discussionmentioning

confidence: 99%

“…In a prostate cancer patient cohort, cofilin levels were increased and they were significantly higher in metastases than in primary tumors [ 33 ]. Cofilin level was also increased in bladder cancer [ 34 ], and in ovarian [ 35 ] and pancreatic cancer [ 36 ] overexpression of cofilin was associated with poor prognosis. In non-small-cell lung cancer (NSCLC) high cofilin level correlated with poor outcome and cisplatin treatment resistance [ 37 ].…”

Section: Introductionmentioning

confidence: 99%

Alendronate-induced disruption of actin cytoskeleton and inhibition of migration/invasion are associated with cofilin downregulation in PC-3 prostate cancer cells

et al. 2018

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Bisphosphonates are used for prevention of osteoporosis and metastatic bone diseases. Anti-invasive effects on various cancer cells have also been reported, but the mechanisms involved are not well-understood. We investigated the effects of the nitrogen-containing bisphosphonate alendronate (ALN) on the regulation of actin cytoskeleton in PC-3 cells. We analyzed the ALN effect on the organization and the dynamics of actin, and on the cytoskeleton-related regulatory proteins cofilin, p21-associated kinase 2 (PAK2), paxillin and focal adhesion kinase. Immunostainings of cofilin in ALN-treated PC-3 cells and xenografts were performed, and the role of cofilin in ALN-regulated F-actin organization and migration/invasion in PC-3 cells was analyzed using cofilin knockdown and transfection. We demonstrate that disrupted F-actin organization and decreased cell motility in ALN-treated PC-3 cells were associated with decreased levels of total and phosphorylated cofilin. PAK2 levels were also lowered but adhesion-related proteins were not altered. The knockdown of cofilin similarly impaired F-actin organization and decreased invasion of PC-3 cells, whereas in the cells transfected with a cofilin expressing vector, ALN treatment did not decrease cellular cofilin levels and migration as in mock transfected cells. ALN also reduced immunohistochemical staining of cofilin in PC-3 xenografts. Our results suggest that reduction of cofilin has an important role in ALN-induced disruption of the actin cytoskeleton and inhibition of the PC-3 cell motility and invasion. These data also support the idea that the nitrogen-containing bisphosphonates could be efficacious in inhibition of prostate cancer invasion and metastasis, if delivered in a pharmacological formulation accessible to the tumors.

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“…Inhibition of ARPC4 expression also led to the attenuation of proliferation, migration and invasion in these cells. 28 Wang et al 29 showed that both miR-182-5p and TCF7L2 30 were involved in the proliferation, migration, and invasion of bladder cancer cell through cofilin-1. Together these findings support a role for ARPC4, not only in the growth of bladder cancer but also in the tumor invasion and metastasis.…”

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confidence: 99%

ARPC4 promotes bladder cancer cell invasion and is associated with lymph node metastasis

et al. 2019

J of Cellular Biochemistry

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The significance of actin‐related protein 2/3 complex subunit 4 (ARPC4) expression in bladder cancer, and its potential role in the invasion and migration of bladder cancer cells, has yet to be determined. This study was to identify the correlation between ARPC4 and lymph node metastasis, and to determine the role of ARPC4 in the invasive migration of T24 bladder cancer cells. One hundred and ninety‐eight bladder cancer tissues and 40 normal bladder and lymph node tissues were examined. Tissue microarrays were constructed and subjected to immunohistochemical stating for ARPC4. Multiple logistic analysis was used to determine risk factors associated with bladder cancer metastasis. ARPC4 expression in T24 bladder cancer cells was suppressed using small interfering RNA and changes in protein levels were determined by Western blot analysis. The proliferation of bladder cancer cells after knocking down of ARPC4 was determined by cell counting kit‐8. The effects of ARPC4 knockdown on T24 cell invasion and migration was determined using transwell and wound healing assays. Immunofluorescence analysis was performed to examine changes in pseudopodia formation and actin cytoskeleton structure. The expression of ARPC4 was elevated in bladder cancer tissues than normal tissues (84.3% vs 27.5%, P < 0.001). The multivariate logistic analysis demonstrated that the level of ARPC4, as a risk factor, was correlated with lymphatic metastasis (P < 0.05). ARPC4 knockdown attenuated proliferation, migration, invasion, and pseudopodia formation in T24 cells. ARPC4 expression, as a risk factor, is associated with lymphatic metastasis and is upregulated in bladder cancer tissues in comparison with normal tissues. Inhibition of ARPC4 expression significantly attenuates the proliferation, migration, and invasion of bladder cancer cell, possibly due to defects in pseudopodia formation.

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Study on the Significance of Cofilin 1 Overexpression in Human Bladder Cancer

Abstract: Our study indicates that Cofilin 1 holds an important position in the development and progression of human bladder cancer, and this gene might become a novel target in the diagnosis and treatment of human bladder cancer.

Cited by 8 publications

References 18 publications

Cofilin 1 promotes bladder cancer and is regulated by TCF7L2

Cofilin 1 promotes bladder cancer and is regulated by TCF7L2

Alendronate-induced disruption of actin cytoskeleton and inhibition of migration/invasion are associated with cofilin downregulation in PC-3 prostate cancer cells

ARPC4 promotes bladder cancer cell invasion and is associated with lymph node metastasis

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