LncRNA LINC01503 aggravates the progression of cervical cancer through sponging miR-342-3p to mediate FXYD3 expression
Autor: | Jinyu Gao, Yumei Zhang, Xing Peng, Chunyan Cai |
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Jazyk: | angličtina |
Rok vydání: | 2020 |
Předmět: |
0301 basic medicine
Biophysics Uterine Cervical Neoplasms Endogeny Apoptosis Biology Malignancy LINC01503 Biochemistry 03 medical and health sciences 0302 clinical medicine Cell Movement medicine Humans Neoplasm Invasiveness Molecular Biology Psychological repression Research Articles Cancer miR-342-3p Cell Proliferation Cervical cancer Oncogene Cell growth Membrane Proteins Cell Biology medicine.disease CC Neoplasm Proteins Gene Expression Regulation Neoplastic MicroRNAs 030104 developmental biology 030220 oncology & carcinogenesis Cancer research Molecular mechanism Disease Progression Female RNA Long Noncoding FXYD3 HeLa Cells Signal Transduction |
Zdroj: | Bioscience Reports |
ISSN: | 1573-4935 0144-8463 |
Popis: | Cervical cancer (CC), an aggressive malignancy, has a high risk of relapse and death, mainly occurring in females. Accumulating investigations have confirmed the critical role of long noncoding RNAs (lncRNAs) in diverse cancers. LncRNA LINC01503 has been reported as an oncogene in several cancers. Nonetheless, its role and molecular mechanism in CC have not been explored. In the present study, we found that FXYD3 expression was considerably up-regulated in CC tissues and cells. Moreover, FXYD3 deficiency conspicuously hampered cell proliferation and migration while facilitated cell apoptosis in CC cells. Subsequently, molecular mechanism experiments implied that FXYD3 was a downstream target gene of miR-342-3p, and FXYD3 expression was reversely mediated by miR-342-3p. Moreover, we discovered that LINC01503 acted as the endogenous sponge for miR-342-3p. Besides, LINC01503 negatively regulated miR-342-3p expression and positively regulated FXYD3 expression in CC. Rescue assays revealed that LINC01503 depletion-induced repression on CC progression could be partly recovered by miR-342-3p inhibition, and then the co-transfection of sh-FXYD3#1 rescued this effect. Conclusively, LINC01503 aggravated CC progression through sponging miR-342-3p to mediate FXYD3 expression, providing promising therapeutic targets for CC patients. |
Databáze: | OpenAIRE |
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