RETRACTED ARTICLE: Long non-coding RNA LINC00525 regulates the proliferation and epithelial to mesenchymal transition of human glioma cells by sponging miR-338-3p
Yilv Wan, Feng Liang, Minjun Wei, Ying Liu
Abstract
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Yilv Wan, Feng Liang, Minjun Wei, Ying Liu
Abstract
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Long non-coding RNA (LncRNA) LINC00525 has been shown to be upregulated in several human cancers and deduced to possess caner regulatory role. The regulation of molecular mechanics of human glioma by lncRNA-LINC00525 through microRNA sponging in glioma is elusive. The lncRNA-LINC00525 showed significant (P < 0.05) upregulation in glioma cancer cells. The upregulation of lncRNA-LINC00525 was upto 6.6-fold in glioma cells relative to the normal cells. Knockdown of lncRNA-LINC00525 significantly declined the proliferation of the glioma cancer cells. Additionally, the colony formation was inhibited by around 60% in glioma cells. The wound healing and transwell assays revealed significant (P < 0.05) inhibition of migration and invasion potential under lncRNA-LINC00525 knockdown. The western blotting study of biomarkers of epithelial to mesenchymal transition (EMT) revealed that lncRNA-LINC00525 gene silencing reduced the expression of mesenchymal molecular markers but increased the protein levels of epithelial markers. miR-338-3p was predicted to be interacting with lncRNA-LINC00525 in glioma and was shown to mediated the regulatory role of lncRNA-LINC00525. Taken together, the results of present study are supportive of the prognostic applicability of lncRNA-LINC00525 against human glioma together with its therapeutic potential against the said malignancy.
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Long non-coding RNA (LncRNA) LINC00525 has been shown to be upregulated in several human cancers and deduced to possess caner regulatory role. The regulation of molecular mechanics of human glioma by lncRNA-LINC00525 through microRNA sponging in glioma is elusive. The lncRNA-LINC00525 showed significant (P < 0.05) upregulation in glioma cancer cells. The upregulation of lncRNA-LINC00525 was upto 6.6-fold in glioma cells relative to the normal cells. Knockdown of lncRNA-LINC00525 significantly declined the proliferation of the glioma cancer cells. Additionally, the colony formation was inhibited by around 60% in glioma cells. The wound healing and transwell assays revealed significant (P < 0.05) inhibition of migration and invasion potential under lncRNA-LINC00525 knockdown. The western blotting study of biomarkers of epithelial to mesenchymal transition (EMT) revealed that lncRNA-LINC00525 gene silencing reduced the expression of mesenchymal molecular markers but increased the protein levels of epithelial markers. miR-338-3p was predicted to be interacting with lncRNA-LINC00525 in glioma and was shown to mediated the regulatory role of lncRNA-LINC00525. Taken together, the results of present study are supportive of the prognostic applicability of lncRNA-LINC00525 against human glioma together with its therapeutic potential against the said malignancy.
Key concepts: Glioma, Gene knockdown, Downregulation and upregulation, Gene silencing, Long non-coding RNA, microRNA, Cancer research, Epithelial–mesenchymal transition