Downregulated Expression of the Cyclase-associated Protein 1 (CAP1) Reduces Migration in Esophageal Squamous Cell Carcinoma

Li, Mei; Yang, Xiaojing; Shi, Hui; Ren, Hailong; Chen, Xueyu; Zhang, Shu; Zhu, Junya; Zhang, Jianguo

doi:10.1093/jjco/hyt093

Cited by 25 publications

(25 citation statements)

References 31 publications

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“…Colocalization of CAP1 with F-actin in the leading edge of cells has been involved in metastasis. Moreover, repression of cofilin-1 or CAP1 in metastatic cells inhibited migration [25, 31, 56, 57]. Therefore, not only the high levels of CAP1 and cofilin-1, but also the high ROS production found in G10 could be key events that promote migration and metastasis.…”

Section: Discussionmentioning

confidence: 99%

Reprogramming human A375 amelanotic melanoma cells by catalase overexpression: Reversion or promotion of malignancy by inducing melanogenesis or metastasis

et al. 2016

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Advanced melanoma is the most aggressive form of skin cancer. It is highly metastatic and dysfunctional in melanogenesis; two processes that are induced by H2O2. This work presents a melanoma cell model with low levels of H2O2 induced by catalase overexpression to study differentiation/dedifferentiation processes. Three clones (A7, C10 and G10) of human A375 amelanotic melanoma cells with quite distinct phenotypes were obtained. These clones faced H2O2 scavenging by two main strategies. One developed by clone G10 where ROS increased. This resulted in G10 migration and metastasis associated with the increased of cofilin-1 and CAP1. The other strategy was observed in clone A7 and C10, where ROS levels were maintained reversing malignant features. Particularly, C10 was not tumorigenic, while A7 reversed the amelanotic phenotype by increasing melanin content and melanocytic differentiation markers. These clones allowed the study of potential differentiation and migration markers and its association with ROS levels in vitro and in vivo, providing a new melanoma model with different degree of malignancy.

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Section: Discussionmentioning

confidence: 99%

Reprogramming human A375 amelanotic melanoma cells by catalase overexpression: Reversion or promotion of malignancy by inducing melanogenesis or metastasis

et al. 2016

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“…29 Thus, it was not surprising that CAP1 depletion reduced cell motility in several cell types, including cancer cells. [12][13][14]25 In contrast to the reduced motility in some cell types, CAP1 knockdown in HeLa cells, however, actually stimulated cell motility and invasion. 5 The CAP1-knockdown HeLa cells also had increased lamellipodia, which could explain the observed cell migration phenotype.…”

Section: Effects Of Cap1 Depletion On the Actin Cytoskeleton And Cellmentioning

confidence: 92%

Mammalian CAP (Cyclase-associated protein) in the world of cell migration

Zhou

Zhang

Field

2013

Cell Adhesion & Migration

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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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Downregulated Expression of the Cyclase-associated Protein 1 (CAP1) Reduces Migration in Esophageal Squamous Cell Carcinoma

Abstract: These ﬁndings suggest that cyclase-associated protein 1 is involved in the metastasis of esophageal squamous cell carcinoma, and that elevated levels of cyclase-associated protein 1 expression may indicate a poor prognosis for patients with esophageal squamous cell carcinoma.

Cited by 25 publications

References 31 publications

Reprogramming human A375 amelanotic melanoma cells by catalase overexpression: Reversion or promotion of malignancy by inducing melanogenesis or metastasis

Reprogramming human A375 amelanotic melanoma cells by catalase overexpression: Reversion or promotion of malignancy by inducing melanogenesis or metastasis

Mammalian CAP (Cyclase-associated protein) in the world of cell migration

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

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