Association of Cortactin and Fascin-1 Expression in Gastric Adenocarcinoma: Correlation With Clinicopathological Parameters

Tsai, Wen‐Chiuan; Jin, Jong‐Shiaw; Chang, Wei‐Kuo; Chan, De-Chuan; Yeh, Ming–Kung; Cherng, Shiou-Chih; Lin, Li-Fan; Sheu, Lai-Fa; Chao, You‐Chen

doi:10.1369/jhc.7a7235.2007

Cited by 56 publications

(60 citation statements)

References 35 publications

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“…Cortactin overexpression is known to be associated with the development of cancer (7)(8)(9)(10)(11). The overexpression of cortactin obtained by immunohistochemistry in 62.5% cases of colorectal cancer is consistent with previous findings.…”

Section: Discussionsupporting

confidence: 89%

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Localization of cortactin is associated with colorectal cancer development

Hirakawa

Shibata²,

Nakayama³

2009

Int J Oncol

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Abstract. Cortactin is a ubiquitously expressed actin filament (F-actin)-binding protein that stabilizes F-actin networks and promotes actin polymerization by activating the actinrelated protein 2/3 (Arp2/3) complex. Overexpression of cortactin in cancer cells stimulate cell migration, invasion, and experimental metastasis; however, the underlying mechanism in cortactin involvement in tumor progression is not fully understood. Recently, a direct interaction between zonula occludens-1 (ZO-1) and cortactin in epithelial cells was reported. The present study aimed to further clarify the significance of the interaction between cortactin and ZO-1 in cancer progression. Cortactin expression and localization in colorectal human cancer tissues were evaluated by immunohistochemistry and immunofluorescence. Co-immunoprecipitation and immunofluorescence analysis revealed cortactin and ZO-1 interaction and localization in cancer cells. In our study, the localization of cortactin is a crucial marker for lymph node metastasis in colorectal cancer. We show how the localization of cortactin effects cancer development. A molecular interaction between cortactin and ZO-1 in migrating or polarized cancer cells was revealed. This is the first report to show the interaction of cortactin and ZO-1 in colorectal cancer progression. We conclude that localization of cortactin in cancer cells and interaction between ZO-1 and cortactin are crucial for cancer progression.

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Section: Discussionsupporting

confidence: 89%

“…The C-terminal half is composed of an ·-helix domain of unknown function, followed by a proline-serine-threonine-rich region (PST) and Src homology 3 (SH3) domain (6). Gene amplification of CTTN and overexpression of cortactin have been reported in various cancers including colorectal cancer (7)(8)(9)(10)(11).…”

Section: Introductionmentioning

confidence: 99%

Localization of cortactin is associated with colorectal cancer development

Hirakawa

Shibata²,

Nakayama³

2009

Int J Oncol

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“…In addition, the deregulation of FSCN1 has been reported in gastric cancer. Tsai et al (18) revealed that among 60 samples of poorly-differentiated gastric adenocarcinomas, over half exhibited moderate or marked FSCN1 expression. Notably, a higher expression of FSCN1 correlated directly with more-advanced cancer stages and inversely with survival rates, suggesting that aberrant upregulation of FSCN1 may be involved in the progression of gastric adenocarcinomas.…”

Section: A B Cmentioning

confidence: 99%

MicroRNA-133a inhibits proliferation and invasion, and induces apoptosis in gastric carcinoma cells via targeting fascin actin-bundling protein 1

Chen

2012

Molecular Medicine Reports

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Abstract. Fascin actin-bundling protein 1 (FSCN1) is associated with tumor progression. In addition, deregulation of the expression of FSCN1 has been observed in certain types of cancer. However, the detailed role of FSCN1 in gastric cancer remains to be elucidated. In the present study, downregulation of microRNA (miR)-133a and upregulation of FSCN1 were both observed in gastric cancer tissues and cell lines. Functional studies have revealed that miR-133a is able to bind to the 3'-untranslated region of FSCN1 mRNA, and overexpression of miR-133a causes downregulation of FSCN1 expression, while downregulation of miR-133a leads to an increased FSCN1 expression in gastric cancer cells. Furthermore, overexpression of miR-133a inhibited proliferation and invasion, but promoted apoptosis of gastric cancer cells, which may be reversed by upregulation of FSCN1. By contrast, downregulation of miR-133a enhanced proliferation and invasion, but suppressed apoptosis in gastric cancer cells. In conclusion, the anti-oncogenic activity of miR-133a may involve the inhibition of the target gene FSCN1. The present study suggested that miR-133a may be a potential therapeutic target in the treatment of gastric cancer.

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“…In addition, the gene's expression was raised significantly at more progressed stages of cancer. In agreement with this study's results, Tsai et al investigated the correlation of cortactin expression with gastric adenocarcinoma clinical parameters through immunohistochemical and tissue microarray analysis [26]. They determined that cortactin overexpression had a direct relationship with more progressed stages of that cancer.…”

Section: Discussionsupporting

confidence: 76%

How Does the Cortactin Gene Expression Affect Breast Cancer among Iranian Females?

Tutunchi¹,

Saffari²,

Mazaheri³

et al. 2016

ABCR

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Introduction: Breast cancer is the most common cancer in the Iranian female population, and the incidence of the disease is rising. Early detection in association with staging or grading the tumor is the most effective method to increase survival rates. Studies have revealed that cortactin overexpression may play a role in the final stages of tumor progression and affects invasion and cellular motility. The aim of this study is to evaluate cortactin gene expression among Iranian female patients with breast cancer. Materials and Methods: Samples belonging to 70 breast cancer patients were randomly selected from the Imam Khomeini tumor bank. Normal and tumor tissues were prepared and stored at −80˚C. Cortactin gene expression was evaluated by real-time PCR. Finally the data, along with demographic and clinical parameters, were analyzed using Prism 5.0 software, followed by t-test and ANOVA analysis. Results: Cortactin gene expression among tumor tissues increased 95.71% in comparison with normal tissues. A significant correlation between cortactin gene expression and lymph nodes' involvement (P = 0.0077) and tumor stage (P = 0.0030) was observed. However, tumor grade (P = 0.8598), tumor size (P = 0.3058), and patient's age (P = 0.4135) had no significant correlation with the gene's expression level. Discussion: This study demonstrated that the cortactin gene's overexpression in breast cancer may enhance lymph nodes' involvement. This study also found that the gene's expression was raised significantly in progressed stages of the cancer. Therefore, cortactin gene overexpression is an important factor indicating breast cells' invasion. Conclusion: The cortactin gene's expression level can be considered an accurate indicator for female breast cancer and also an appropriate biomarker for this cancer in clinical evaluations.

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Association of Cortactin and Fascin-1 Expression in Gastric Adenocarcinoma: Correlation With Clinicopathological Parameters

Cited by 56 publications

References 35 publications

Localization of cortactin is associated with colorectal cancer development

Localization of cortactin is associated with colorectal cancer development

MicroRNA-133a inhibits proliferation and invasion, and induces apoptosis in gastric carcinoma cells via targeting fascin actin-bundling protein 1

How Does the Cortactin Gene Expression Affect Breast Cancer among Iranian Females?

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