Silencing of COX-2 by RNAi Modulates Epithelial-Mesenchymal Transition in Breast Cancer Cells Partially Dependent on the PGE<sub>2</sub>Cascade

Cao, Juan; Xiao, Yang; Li, Wentong; Zhao, Chunling; Lv, Shijun

doi:10.7314/apjcp.2014.15.22.9967

Cited by 4 publications

(4 citation statements)

References 33 publications

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“…In previous studies, PGE2 significantly promoted proliferation and invasion by upregulating the expression of survivin (5), focal adhesion kinase (4), Snail (6,7), YB-1 (8), c-Myc (9) and β1-integrin (10) in hepatocellular carcinoma cells, and by upregulating the expression of MMP2 (11) and the FUSE-binding protein 1 (12) in cholangiocarcinoma cells. It was also reported that, PGE2 promoted cell proliferation and invasion in breast (13), colon (14), ovarian (15) cancer and several other types of tumors.…”

Section: Introductionmentioning

confidence: 85%

Prostaglandin E2 promotes human cholangiocarcinoma cell proliferation, migration and invasion through the upregulation of β-catenin expression via EP3-4 receptor

Feng

Zhang

et al. 2015

Oncology Reports

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Abstract. Prostaglandin E2 (PGE2) is involved in cholangiocarcinoma cell proliferation, migration and invasion through E prostanoid receptors, including EP1, EP2 and EP4. However, the functions and the mechanisms of those splice variants of EP3 receptors in promoting liver cancer cell growth and invasion remain to be elucidated. In our previous studies, four isoforms of EP3 receptors, EP3-4, EP3-5, EP3-6 and EP3-7 receptors, were detected in CCLP1 and HuCCT1 cells. However, the functions of these receptors in these cells have yet to be determined. It was reported that β-catenin is closely correlated with malignancy, including cholangiocarcinoma. The present study was designed to examine the effects of 4-7 isoforms of EP3 in promoting cholangiocarcinoma progression and the mechanisms by which PGE2 increases β-catenin protein via EP3 receptors. The results showed that PGE2 promotes cholangiocarcinoma progression via the upregulation of β-catenin protein, and the EP3-4 receptor pathway is mainly responsible for this regulation. These findings reveal that PGE2 upregulated the cholangiocarcinoma cell β-catenin protein through the EP3-4R/Src/EGFR/PI3K/AKT/GSK-3β pathway. The present study identified the functions of EP3 and the mechanisms by which PGE2 regulates β-catenin expression and promoted cholangiocarcinoma cell growth and invasion.

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Section: Introductionmentioning

confidence: 85%

Prostaglandin E2 promotes human cholangiocarcinoma cell proliferation, migration and invasion through the upregulation of β-catenin expression via EP3-4 receptor

Feng

Zhang

et al. 2015

Oncology Reports

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“…Also, metastasis is a multistep process involving cell detachment from the primary tumor, extravasation, and invasion to the secondary organ (Lv et al, 2011;Li et al, 2014). During the metastasis process, the oncogenes are activated and the tumor suppressor genes are inactivated, which may be responsible for breast cancer metastasis (Hong et al, 2012;Liu et al, 2013;Cao et al, 2014). Promoter hypermethylation of tumor suppressor genes is one of the ways to suppress its expression during the breast cancer metastasis (Lv et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

Hypermethylation of TET1 Promoter Is a New Diagnosic Marker for Breast Cancer Metastasis

Sang

Cheng²,

Tang³

et al. 2015

Asian Pacific Journal of Cancer Prevention

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Breast cancer metastasis is a major cause of cancer-related death in women. However, markers for diagnosis of breast cancer metastasis are rare. Here, we reported that TET1, a tumor suppressor gene, was downregulated and hypermethylated in highly metastatic breast cancer cell lines. Moreover, silencing of TET1 in breast cancer cells increased the migration and spreading of breast cancer cells. In breast cancer clinical samples, TET1 expression was reduced in LN metastases compared with primary tissues. Besides, the methylation level of the TET1 promoter was increased significantly in LN metastases. Taken together, these findings indicate that promoter hypermethylation may contribute to the downregulation of TET1 and could be used as a promising marker for diagnosis in patients with breast cancer metastasis.

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“…It is critical for breast cancer management to identify those biomarkers that would provide, at the time of diagnosis, a reliable prognostic assessment and prediction of treatment response (Diers et al, 2013;Cao et al, 2014;Witteveen et al, 2015). Several studies have shown that COX-2 is implicated in carcinogenesis and tumor progression in many human cancers, including breast cancer.…”

Section: Discussionmentioning

confidence: 99%

COX-2 expression correlation with invasion in human breast carcinomas and in cell line MDA-MB-231 in vitro

Wang

Chen

et al. 2016

Bangladesh J Pharmacol

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COX-2 expression by means of immunohistochemistry in 120 cases breast invasive ductal carcinomas and 60 cases benign lesions were compared with clinicopathological features and prognostic molecular markers. COX-2 role of invasiveness and chemotaxis in breast cancer cell line MDA-MB-231 by using small RNA interference (siRNA) plasmids to disrupt COX-2 expression in vitro were investigated. The results show that COX-2 immune positivity and percentage of positive cells in breast carcinomas were higher than those in benign lesions and positivity correlated significantly with HIF-1?, VEGF, the grading, metastasis and vascular invasion of carcinoma (p<0.05). This study suggests that COX-2 overexpression correlates with poor clinicopathological parameters in breast cancers, and the reduction of COX-2 expression can obviously inhibit the invasion and chemotaxis of cancer cell line MDA-MB-231 using RNA interference. The findings of the present study suggest that COX-2 overexpression in breast cancer may be considered as a negative prognostic marker.

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Silencing of COX-2 by RNAi Modulates Epithelial-Mesenchymal Transition in Breast Cancer Cells Partially Dependent on the PGE₂Cascade

Cited by 4 publications

References 33 publications

Prostaglandin E2 promotes human cholangiocarcinoma cell proliferation, migration and invasion through the upregulation of β-catenin expression via EP3-4 receptor

Prostaglandin E2 promotes human cholangiocarcinoma cell proliferation, migration and invasion through the upregulation of β-catenin expression via EP3-4 receptor

Hypermethylation of TET1 Promoter Is a New Diagnosic Marker for Breast Cancer Metastasis

COX-2 expression correlation with invasion in human breast carcinomas and in cell line MDA-MB-231 in vitro

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Silencing of COX-2 by RNAi Modulates Epithelial-Mesenchymal Transition in Breast Cancer Cells Partially Dependent on the PGE2Cascade

Cited by 4 publications

References 33 publications

Prostaglandin E2 promotes human cholangiocarcinoma cell proliferation, migration and invasion through the upregulation of β-catenin expression via EP3-4 receptor

Prostaglandin E2 promotes human cholangiocarcinoma cell proliferation, migration and invasion through the upregulation of β-catenin expression via EP3-4 receptor

Hypermethylation of TET1 Promoter Is a New Diagnosic Marker for Breast Cancer Metastasis

COX-2 expression correlation with invasion in human breast carcinomas and in cell line MDA-MB-231 in vitro

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Silencing of COX-2 by RNAi Modulates Epithelial-Mesenchymal Transition in Breast Cancer Cells Partially Dependent on the PGE₂Cascade