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Cellular proliferation of Hemangioma endothelial cells (HemECs) under targeted regulation of LncRNA MALAT1 via miR-494-3p/PTEN Axis

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The current study is aimed to explore the regulation of lncRNA MALAT1 in human HemECs functions. In our study, relative expressions of MALAT1, miR-494-3p and PTEN in HemECs (HemEC) were determined using qRT-PCR methods. MTT assays were used to measure cell viability. The rate of cell apoptosis was assessed using caspase-3 assay. Transfections were performed to mediate lncRNA MALAT1 and miR-494-3p expression in HemEc cells. Also, Bioinformatic analysis and Luciferase reporter were used to predict and validate the bindings between MALAT1 and PTEN, and PTEN and miR-494-3-p. MALAT1 was highly expressed in HemECs. Cell proliferation increased significantly due to MALAT1 overexpression in HemECs while MALAT1 overexpression significantly reduced cell apoptosis in HemECs. On the other hand, contradictory results were observed due to the reduction of MALAT1 in HemEC. We also found that MALAT1 interacts with miR-494-3p/PTEN to mediate cellular functions. Collectively, the results showed that the MALAT1 expression was negatively associated with miR-494-3p and positively matched the PTEN expression. In addition, MALAT1 acted as a ceRNA by binding with miR-494-3p to up-regulate PTEN in HemECs. Our study showed that MALAT1 accelerates the proliferation of HemEC cells by controlling the miR-494-3p/PTEN axis promoting new insight into IH treatment.
Title: Cellular proliferation of Hemangioma endothelial cells (HemECs) under targeted regulation of LncRNA MALAT1 via miR-494-3p/PTEN Axis
Description:
The current study is aimed to explore the regulation of lncRNA MALAT1 in human HemECs functions.
In our study, relative expressions of MALAT1, miR-494-3p and PTEN in HemECs (HemEC) were determined using qRT-PCR methods.
MTT assays were used to measure cell viability.
The rate of cell apoptosis was assessed using caspase-3 assay.
Transfections were performed to mediate lncRNA MALAT1 and miR-494-3p expression in HemEc cells.
Also, Bioinformatic analysis and Luciferase reporter were used to predict and validate the bindings between MALAT1 and PTEN, and PTEN and miR-494-3-p.
MALAT1 was highly expressed in HemECs.
Cell proliferation increased significantly due to MALAT1 overexpression in HemECs while MALAT1 overexpression significantly reduced cell apoptosis in HemECs.
On the other hand, contradictory results were observed due to the reduction of MALAT1 in HemEC.
We also found that MALAT1 interacts with miR-494-3p/PTEN to mediate cellular functions.
Collectively, the results showed that the MALAT1 expression was negatively associated with miR-494-3p and positively matched the PTEN expression.
In addition, MALAT1 acted as a ceRNA by binding with miR-494-3p to up-regulate PTEN in HemECs.
Our study showed that MALAT1 accelerates the proliferation of HemEC cells by controlling the miR-494-3p/PTEN axis promoting new insight into IH treatment.

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