Background: Although SCIRT has been reported to suppress breast cancer, its role in other cancers, such as oral squamous cell carcinoma (OSCC), is hardly known. We predicted that SCIRT might interact with miR-221 to target lncRNA GAS5 and analyzed the interaction between SCIRT and miR-221 in OSCC.
Methods: SCIRT and miR-221 expression levels were quantified using RT-qPCR. SCIRT subcellular localization was analyzed by subcellular fractionation assay. RNA pull-down assay was applied to study the interaction between SCIRT and miR-221. The role of SCIRT and miR-221 in regulating GAS5 expression was analyzed by overexpression assay and RT-qPCR. Cell apoptosis was analyzed by flow cytometry.
Results: SCIRT and GAS5 were downregulated, while miR-221 was overexpressed in OSCC. SCIRT was detected in both nucleus and cytoplasm and directly interacted with miR-221, while SCIRT overexpression failed to affect miR-221 expression. In addition, GAS5 expression was increased by SCIRT and decreased by miR-221. Moreover, SCIRT suppressed the role of miR-221 in suppressing GAS5 expression and OSCC cell apoptosis.
Conclusion: SCIRT sponges miR-221 to upregulate lncRNA GAS5 in OSCC and inhibit cancer cell apoptosis.
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http://dx.doi.org/10.1111/jop.13241 | DOI Listing |
J Oral Pathol Med
March 2022
Department of Stomatology, The Fourth Hospital of Hebei Medical University, Shijiazhuang, China.
Background: Although SCIRT has been reported to suppress breast cancer, its role in other cancers, such as oral squamous cell carcinoma (OSCC), is hardly known. We predicted that SCIRT might interact with miR-221 to target lncRNA GAS5 and analyzed the interaction between SCIRT and miR-221 in OSCC.
Methods: SCIRT and miR-221 expression levels were quantified using RT-qPCR.
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