Abstract
BackgroundThyroid cancer (TC) is a member of common malignant tumors in endocrine system. To develop effective treatment, further comprehension of understanding molecular mechanism in TC is necessary. In this research, we attempted to search the underlying molecular mechanism in TC.MethodsZEB1-AS1 expression was analyzed via qRT-PCR analysis. CCK-8, colony formation, flow cytometry and TUNEL assays were used to evaluate TC cell growth. The interaction between miR-133a-3p and LPAR3, EGFR and ZEB1-AS1 was testified through using RNA pull down and luciferase reporter assays.ResultsLPAR3 and EGFR were expressed at high levels in TC tissues and cell lines. Besides, both LPAR3 and EGFR could promote TC cell growth. Later, miR-133a-3p was searched as an upstream gene of LPAR3 and EGFR, and LPAR3 could partially rescue the suppressive effect of miR-133a-3p overexpression on TC progression, whereas the co-transfection of LPAR3 and EGFR completely restored the inhibition. Next, ZEB1-AS1 was confirmed as a sponge of miR-133a-3p. ZEB1-AS1 has a negative correlation with miR-133a-3p and a positive association with LPAR3 and EGFR through ceRNA analysis. Importantly, ZEB1-AS1 boosted the proliferation and suppressed the apoptosis in TC cells. Through restoration assays, we discovered that ZEB1-AS1 regulated LPAR3 and EGFR expression to mediate TC cell proliferation and apoptosis by sponging miR-133a-3p. Further investigation also indicated the oncogenic role of ZEB1-AS1 by mediating PI3K/AKT/mTOR pathway.ConclusionsZEB1-AS1 could be an underlying biomarker in TC.
Highlights
Thyroid cancer (TC) is a member of common malignant tumors in endocrine system
The oncogenic role of Lysophosphatidic acid receptor 3 (LPAR3) and epidermal growth factor receptor (EGFR) was revealed in TC, and we found ZEB1-AS1/miR133a-3p/LPAR3/EGFR axis, which promoted TC progression by regulating PI3K/AKT/mTOR pathway
LPAR3 and EGFR are overexpressed in TC tissues and cells Through quantitative real-time polymerase chain reaction (qRT-PCR) assay, we observed that the expression of LPAR3 and EGFR was markedly higher in TC tissues than that in matched adjacent tissues (Fig. 1a)
Summary
Thyroid cancer (TC) is a member of common malignant tumors in endocrine system. Further comprehension of understanding molecular mechanism in TC is necessary. We attempted to search the underlying molecular mechanism in TC. Thyroid cancer (TC) is a type of cancer in endocrine system and serves as a malignant tumor occurred in the patients [1]. More than 90% of TCs are caused by follicular cells, which are epithelial cells that act on uptaking iodine and synthesizing thyroid hormone [3]. Long non-coding RNAs (lncRNAs) are a group of RNA molecules with a limit in coding proteins and more than 200 nucleotides (nt) in length. Mounting reports have suggested that lncRNAs appear as important regulators in numerous biological processes [6].
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