Anticancer research · 2023
Long Non-coding RNA LINC00152 Requires EZH2 to Promote Mesothelioma Cell Proliferation, Migration, and Invasion.
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Endo Ihiro, Amatya Vishwa Jeet, Kushitani Kei, Nakagiri Tetsuya, Aoe Kohei, Takeshima Yukio
Аннотация
BACKGROUND/AIM: Long non-coding RNAs (lncRNAs) establish gene regulatory networks in different human cancers and are involved in tumorigenesis. lncRNA LINC00152 is over-expressed in several malignant tumors and involved in tumorigenesis; however, its underlying regulatory mechanisms remain unclear. Mesothelioma, a cancer originating from mesothelial cells, is highly aggressive with a poor prognosis. Therefore, identification of new therapeutic targets is necessary for mesothelioma treatment.
MATERIALS AND METHODS: Here, we conducted bioinformatics analyses of LINC00152 and enhancer of zeste homolog 2 (EZH2) expression levels and their correlation with the prognosis of patients with mesothelioma. Small interfering RNAs targeting LINC00152 and EZH2 were transfected into mesothelioma cell lines to analyze their biological functions and regulatory mechanisms.
RESULTS: High LINC00152 expression was associated with a poor prognosis of patients with mesothelioma. LINC00152 knockdown inhibited the proliferation, migration, and invasion of mesothelioma cell lines. These results suggest that LINC00152 is a tumor-promoting factor in mesothelioma. EZH2 is highly expressed in mesothelioma and other malignancies. Direct interaction between LINC00152 and EZH2 is associated with cancer development and progression. When EZH2 expression was suppressed, LINC00152 knockdown did not suppress the proliferation, migration, and invasion of mesothelioma cells. Therefore, the tumor-promoting effect of LINC00152 in mesothelioma was dependent on EZH2 expression.
CONCLUSION: LINC00152 promotes mesothelioma cell proliferation, migration, and invasion in cooperation with EZH2, highlighting its potential as an effective therapeutic target for mesothelioma.
MATERIALS AND METHODS: Here, we conducted bioinformatics analyses of LINC00152 and enhancer of zeste homolog 2 (EZH2) expression levels and their correlation with the prognosis of patients with mesothelioma. Small interfering RNAs targeting LINC00152 and EZH2 were transfected into mesothelioma cell lines to analyze their biological functions and regulatory mechanisms.
RESULTS: High LINC00152 expression was associated with a poor prognosis of patients with mesothelioma. LINC00152 knockdown inhibited the proliferation, migration, and invasion of mesothelioma cell lines. These results suggest that LINC00152 is a tumor-promoting factor in mesothelioma. EZH2 is highly expressed in mesothelioma and other malignancies. Direct interaction between LINC00152 and EZH2 is associated with cancer development and progression. When EZH2 expression was suppressed, LINC00152 knockdown did not suppress the proliferation, migration, and invasion of mesothelioma cells. Therefore, the tumor-promoting effect of LINC00152 in mesothelioma was dependent on EZH2 expression.
CONCLUSION: LINC00152 promotes mesothelioma cell proliferation, migration, and invasion in cooperation with EZH2, highlighting its potential as an effective therapeutic target for mesothelioma.