MUC16 (CA125) regulates epithelial ovarian cancer cell growth, tumorigenesis and metastasis

Thériault, Catherine; Pinard, Maxime; Comamala, Marina; Migneault, Martine; Beaudin, Julie; Matte, Isabelle; Boivin, Micheline; Piché, Alain; Rancourt, Claudine

doi:10.1016/j.ygyno.2011.02.020

Cited by 157 publications

(151 citation statements)

References 44 publications

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“…The contribution of MUC16 to cancer malignancy has been studied in many cancer types. Silencing MUC16 studies in ovarian, breast, and pancreatic cancer cells impairs tumorigenic and metastatic properties (36)(37)(38). Moreover, MUC16 rendered antiapoptotic properties to cancer cells, leading to chemotherapy resistance (39).…”

Section: Discussionmentioning

confidence: 99%

Oncogenic KRAS Targets MUC16/CA125 in Pancreatic Ductal Adenocarcinoma

Liang

Qin

Zhang

et al. 2017

Molecular Cancer Research

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Section: Discussionmentioning

confidence: 99%

Oncogenic KRAS Targets MUC16/CA125 in Pancreatic Ductal Adenocarcinoma

Liang

Qin

Zhang

et al. 2017

Molecular Cancer Research

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“…Furthermore, data from our laboratory suggest that ascites stimulates the expression and release of MUC16 from the mesothelial cell membranes [38]. MUC16 is an oncogenic high molecular weight mucin that promotes EOC progression [39][40][41][42] and regulates the formation of multicellular spheroids [43]. Therefore, through ascites exposure, myoibroblastic-like cells become a major source of secreted factors, which in turn, further contribute to the evolution of the tumor environment.…”

Section: Cellular Contents: Contribution To Eoc Metastasismentioning

confidence: 99%

Ascites in Ovarian Cancer Progression: Opportunities for Biomarker Discovery and New Avenues for Targeted Therapies

Matte¹,

Bessette²,

Piché³

2017

Ascites - Physiopathology, Treatment, Complications and Prognosis

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Until recently, ovarian cancer research has mainly focused on the tumor cell themselves ignoring for the most part the surrounding tumor environment. However, one of the major conceptual advances in oncology over the last few years has been the appreciation that major aspects of cancer biology are inluenced by the tumor environment. Malignant ascites accumulates in the peritoneal cavity during ovarian cancer progression and constitutes a unique pro-inlammatory tumor environment providing a framework that orchestrates cellular and molecular changes contributing to aggressiveness and disease progression. The composition of ascites, which includes cellular and acellular components, constantly adapts during the course of the disease in response to various cellular cues originating from both tumor and stromal cells. Increasing evidence now supports an active role of ascites in the progression of ovarian cancer. Although much work is still needed to fully understand the contribution of ascites to ovarian cancer aggressiveness, this tumor environment potentially provides a wealth of opportunities for translational research including biomarker discovery and novel therapeutic target identiication. In this review, we discuss recent advances in our understanding of ascites pathophysiology, the characterization of its cellular and acellular contents, the intercellular crosstalks, and how these data can be used to improve the outcome of ovarian cancer.

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“…This is especially important given that the molecular makeup of tumor cells changes dynamically during progression through the process of Epithelial-to-Mesenchymal Transition (EMT) and its reverse process, Mesenchymalto-Epithelial Transition (MET). It has been shown that EMT in ovarian cancer is controlled by different cytokines and growth factors, such as mucin (MUC4) and CA125 (Ponnusamy et al 2010;Theriault et al 2011), bone morphogenetic protein 4 (BMP4), endothelin-1 (ET-1), epidermal growth factor (EGF), hepatocyte growth factor (HGF) and transforming growth factor-β (TGF-β) (Vergara et al 2010). More recently in an in vitro study, thrombin induced the expression of EMT proteins in EOC cells (Skov-3), which could be reversed with the use of inhibitors against thrombin (hirudin); this indicates that the use of anticoagulants might serve in the control of EOC progression (Zhong et al 2013).…”

Section: Introductionmentioning

confidence: 99%

Immunohistological Insight into the Correlation between Neuropilin-1 and Epithelial-Mesenchymal Transition Markers in Epithelial Ovarian Cancer

Adham

Al-Harrasi

Haddabi

et al. 2014

J Histochem Cytochem.

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The mechanism by which neuropilin-1 (NRP-1) induces malignancy in Epithelial Ovarian Cancer (EOC) is still unknown. This study is the first to demonstrate the relationship between NRP-1 expression and EMT markers vimentin, N-cadherin, E-cadherin and Slug. We used tissue microarrays containing the three main subtypes of EOC tumors: serous, mucinous cystadenocarcinoma and endometrioid adenocarcinoma and representative cases retrieved from our pathology archives. Immunohistochemistry was performed to detect the expression levels and location of NRP-1 and the aforementioned EMT proteins. NRP-1 was mainly expressed on cancer cells but not in normal ovarian surface epithelium (OSE). The Immunoreactive Scoring (IRS) values revealed that the expression of NRP-1, Slug and E-cadherin in the malignant subtypes of ovarian tissues was significantly higher (5.18 ± 0.64, 4.84 ± 0.7, 4.98 ± 0.68, respectively) than their expression in the normal and benign tissues (1.04 ± 0.29, 0.84 ± 0.68, 1.71 ± 0.66, respectively), with no significant differences among the studied subtypes. Vimentin was expressed in the cancer cell component of 43% of tumors and it was exclusively localized in the stroma of all mucinous tumors. The Spearman’s rho value indicated that NRP-1 is positively related to the EMT markers E-cadherin and Slug. This notion might indicate that NRP-1 is a partner in the EMT process in EOC tumors.

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MUC16 (CA125) regulates epithelial ovarian cancer cell growth, tumorigenesis and metastasis

Cited by 157 publications

References 44 publications

Oncogenic KRAS Targets MUC16/CA125 in Pancreatic Ductal Adenocarcinoma

Oncogenic KRAS Targets MUC16/CA125 in Pancreatic Ductal Adenocarcinoma

Ascites in Ovarian Cancer Progression: Opportunities for Biomarker Discovery and New Avenues for Targeted Therapies

Immunohistological Insight into the Correlation between Neuropilin-1 and Epithelial-Mesenchymal Transition Markers in Epithelial Ovarian Cancer

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