PCAT1 is a poor prognostic factor in endometrial carcinoma and associated with cancer cell proliferation, migration and invasion.

Zhao X, Fan Y, Lu C, Li H, Zhou N, Sun G, Fan H
Bosnian journal of basic medical sciences · 2019 · doi:10.17305/bjbms.2019.4096 · PMID:31136293 · PMC6716094
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This study identifies PCAT1 as a poor prognostic factor in endometrial carcinoma, demonstrating that its elevated expression correlates with advanced disease stages and shorter survival while promoting cancer cell proliferation, migration, and invasion.

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This study investigated the clinical significance and biological function of prostate cancer-associated transcript 1 (PCAT1) in endometrial carcinoma by analyzing 89 tissue samples and four cell lines. The researchers found that elevated PCAT1 expression correlated with advanced FIGO stage, myometrial invasion, lymph node metastasis, and shorter overall survival. Functional assays demonstrated that silencing PCAT1 suppressed cell proliferation, migration, and invasion while promoting apoptosis through the regulation of Bcl-2, vimentin, N-cadherin, E-cadherin, and Bad proteins. This paper is centrally about endometriosis and adenomyosis research? No, this paper focuses exclusively on endometrial carcinoma, a distinct malignancy of the uterine lining, rather than the benign conditions endometriosis or adenomyosis; it was included in the corpus via a keyword match in the upstream search index.

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Abstract

Long non-coding RNAs (lncRNAs) are emerging as important modulators of cancer progression, among which prostate cancer-associated transcript 1 (PCAT1) has been shown to be an oncogene in several tumors. However, the clinical significance and biological function of PCAT1 in endometrial carcinoma (EC) remain unclear. In this study, we used 89 EC tissues and HEC-1B, Ishikawa, RL95-2 and AN3CA EC cell lines. We found elevated expression levels of PCAT1 in EC tissues and cell lines using reverse transcription qPCR (RT-qPCR). The prognostic value of PCAT1 was determined using Kaplan-Meier survival and Cox regression analysis. The results showed that higher PCAT1 expression was positively correlated with FIGO stage, myometrial invasion, lymph node metastasis, and a shorter overall survival. A series of functional assays showed that the knockdown of PCAT1 by small interfering RNA (siRNA) targeting PCAT1 (siPCAT1) suppressed cell proliferation, migration and invasion, but promoted apoptosis. Western blot analysis further showed that B-cell lymphoma 2 (Bcl-2), vimentin and N-cadherin were downregulated, but E-cadherin and Bcl-2-associated death promoter (Bad) were upregulated in PCAT1-silenced EC cells. Taken together, our results underscore the oncogenic role of PCAT1 in EC and show that PCAT1 may be a potential therapeutic target in EC treatment.
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PCAT1 is a poor prognostic factor in endometrial carcinoma and associated with cancer cell proliferation, migration and invasion DOI: https://doi.org/10.17305/bjbms.2019.4096Keywords: endometrial carcinoma, PCAT1, prognosis, cell proliferation, migration, invasionAbstract Long non-coding RNAs (lncRNAs) are emerging as important modulators of cancer progression, among which prostate cancer-associated transcript 1 (PCAT1) has been shown to be an oncogene in several tumors. However, the clinical significance and biological function of PCAT1 in endometrial carcinoma (EC) remain unclear. In this study, we used 89 EC tissues and HEC-1B, Ishikawa, RL95-2 and AN3CA EC cell lines. We found elevated expression levels of PCAT1 in EC tissues and cell lines using reverse transcription qPCR (RT-qPCR). The prognostic value of PCAT1 was determined using Kaplan–Meier survival and Cox regression analysis. The results showed that higher PCAT1 expression was positively correlated with FIGO stage, myometrial invasion, lymph node metastasis, and a shorter overall survival. A series of functional assays showed that the knockdown of PCAT1 by small interfering RNA (siRNA) targeting PCAT1 (siPCAT1) suppressed cell proliferation, migration and invasion, but promoted apoptosis. Western blot analysis further showed that B-cell lymphoma 2 (Bcl-2), vimentin and N-cadherin were downregulated, but E-cadherin and Bcl-2-associated death promoter (Bad) were upregulated in PCAT1-silenced EC cells. Taken together, our results underscore the oncogenic role of PCAT1 in EC and show that PCAT1 may be a potential therapeutic target in EC treatment. Citations Downloads Downloads Additional Files Published Issue Section Categories How to Cite Accepted 2019-02-04 Published 2019-08-20

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