Knocking down the expression of adenylate cyclase-associated protein 1 inhibits the proliferation and migration of breast cancer cells

Yu, Xiafei; Ni, Qing; Chen, Jinpeng; Xu, Jiacheng; Jiang, Ying; Yang, Shuyun; Ma, Jing; Gu, Xiaoling; Wang, Hua; Wang, Yingying

doi:10.1016/j.yexmp.2014.02.002

Cited by 30 publications

(20 citation statements)

References 31 publications

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“…It has been reported that the knockdown of the expression of CAP1 affects the breast cancer cell cycle, inhibiting the growth of breast cancer cancer ( 25 ). In this study, we found that a high CAP1 expression associated with a poor prognosis of patients with EOC.…”

Section: Resultsmentioning

confidence: 99%

“…It has been reported that CAP1 is upregulated in breast cancer. After knocking down its expression, the proliferation and migration of MDA-MB-231 cells was shown to decrease, inducing changes in morphology, which were associated with the arrangement of F-actin ( 25 ). Western blot analysis, real-time PCR and immunohistochemical analysis have been used to prove that CAP1 is overexpressed in hepatocellular carcinoma compared with adjacent non-cancerous liver tissues, and that it is positively associated with HCC cell metastasis ( 24 ).…”

Section: Discussionmentioning

confidence: 99%

“…On both ends of the actin filament, CAP1 rapidly translocates to the mitochondria upon treatment with agents that induce apoptosis ( 23 ). Studies have demonstrated that CAP1 is overexpressed in hepatocelluar carcinoma ( 24 ), breast cancer ( 25 ), lung cancer ( 26 ) and esophageal squamous cell carcinoma ( 27 ). However, to the best of our knowledge, no more information is available to date regarding the role of CAP1 in ovarian tumorigenesis.…”

Section: Introductionmentioning

confidence: 99%

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CAP1 is overexpressed in human epithelial ovarian cancer and promotes cell proliferation

Mao

Shu

Deng

et al. 2015

International Journal of Molecular Medicine

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Adenylate cyclase-associated protein 1 (CAP1) regulates both actin filaments and the Ras/cAMP pathway in yeast, and has been found play a role in cell motility and in the development of certain types of cancer. In the present study, we investigated CAP1 gene expression in human epithelial ovarian cancer (EOC). Western blot analysis and immunohistochemistry were performed using EOC tissue samples and the results revealed that CAP1 expression increased with the increasing grade of EOC. In the normal ovarian tissue samples however, CAP1 expression was barely detected. Using Pearson’s χ2 test, it was demonstrated that CAP1 expression was associated with the histological grade and Ki-67 expression. Kaplan-Meier analysis revealed that a higher CAP1 expression in patients with EOC was associated with a poorer prognosis. In in vitro experiments using HO-8910 EOC cells, the expression of CAP1 was knocked down using siRNA. The proliferation of the HO-8910 cells was then determined by cell cycle analysis and cell proliferation assay using the cell counting kit-8 and flow cytometry. The results revealed that the loss of CAP1 expression inhibited cell cycle progression. These findings suggest that a high expression of CAP1 is involved in the pathogenesis of EOC, and that the downregulation of CAP1 in tumor cells may be a therapeutic target for the treatment of patients with EOC.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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CAP1 is overexpressed in human epithelial ovarian cancer and promotes cell proliferation

Mao

Shu

Deng

et al. 2015

International Journal of Molecular Medicine

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“…Knockdown of CAP1 leads to reduced cell motility in lung and pancreatic cancer [7, 10]. However, depletion of CAP1 in HeLa cells and breast cancer cells substantially stimulates the migration and invasion [11, 12]. These results indicate that CAP may either play oncogenic or anti-oncogenic function hinging on cancer types.…”

Section: Introductionmentioning

confidence: 99%

Systematic analysis of gene expression alterations and clinical outcomes of adenylate cyclase-associated protein in cancer

et al. 2017

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Adenylate Cyclase-associated protein (CAP) is an evolutionarily conserved protein that regulates actin dynamics. Our previous study indicates that CAP1 is overexpressed in NSCLC tissues and correlated with poor clinical outcomes, but CAP1 in HeLa cells actually inhibited migration and invasion, the role of CAP was discrepancy in different cancer types. The present study aims to determine whether CAP can serve as a prognostic marker in human cancers. The CAP expression was assessed using Oncomine database to determine the gene alteration during carcinogenesis, the copy number alteration, or mutations of CAP using cBioPortal, International Cancer Genome Consortium, and Tumorscape database investigated, and the association between CAP expression and the survival of cancer patient using Kaplan-Meier plotter and PrognoScan database evaluated. Therefore, the functional correlation between CAP expression and cancer phenotypes can be established; wherein CAP might serve as a diagnostic marker or therapeutic target for certain types of cancers.

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“…The N-terminal region of CAP binds to Cyr1 and is associated with Ras responsiveness in yeast (10)(11)(12). The C-terminal region of this protein binds monomeric actin with high affinity, and is necessary for normal cellular morphology (13) Previous research has shown that CAP1 is overexpressed in hepatocellular carcinoma (14), breast (15) and lung cancer (16), and esophageal squamous cell carcinoma (17). Yet, there is sparse research on the influence of CAP1 in gliomas.…”

Section: Introductionmentioning

confidence: 99%

Overexpression of CAP1 and its significance in tumor cell proliferation, migration and invasion in glioma

et al. 2016

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Adenylate cyclase-associated protein 1 (CAP1), a protein related to the regulation of actin filaments and the Ras/cAMP pathway, is associated with tumor progression. Nevertheless, the expression level and effects of CAP1 in regards to glioma have not been reported. In the present study, we examined the expression of CAP1 in glioma and tumor adjacent normal brain tissues by tissue microarray and immunohistochemistry. Our results showed that CAP1 was overexpressed in glioma tissues in comparison with that noted in the tumor adjacent normal brain tissues and increased staining of CAP1 was found to be correlated with WHO stage. In addition, we discovered that knockdown of CAP1 by specific RNA interference markedly inhibited cell growth and caused downregulation of the proliferation markers, PCNA and cyclin A. We further demonstrated that knockdown of CAP1 inhibited cell metastatic abilities by downregulating N-cadherin and vimentin and upregulating E-cadherin. These findings revealed that CAP1 expression is markedly increased in human glioma and that downregulation of CAP1 in tumors may serve as a treatment for glioma patients.

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Knocking down the expression of adenylate cyclase-associated protein 1 inhibits the proliferation and migration of breast cancer cells

Cited by 30 publications

References 31 publications

CAP1 is overexpressed in human epithelial ovarian cancer and promotes cell proliferation

CAP1 is overexpressed in human epithelial ovarian cancer and promotes cell proliferation

Systematic analysis of gene expression alterations and clinical outcomes of adenylate cyclase-associated protein in cancer

Overexpression of CAP1 and its significance in tumor cell proliferation, migration and invasion in glioma

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