Abstract

Long noncoding RNAs (lncRNAs) play an essential role in the progression of papillary thyroid cancer (PTC). However, the expression and function of lncRNA cancer susceptibility candidate 7 (CASC7) in PTC remain unknown. The purpose of this study was to investigate the role and molecular mechanism of CASC7 in regulating PTC cell behavior. The expression of CASC7, miR-34a-5p, and tumor protein P73 (TP73) was determined by qRT-PCR and western blot. Cell proliferation was examined by MTT assay. Cell apoptosis was assessed by flow cytometry following Annexin V and PI staining. Cell migration was determined by Transwell migration assay. The interaction between miR-34a-5p and CASC7 or TP73 was examined by luciferase reporter assay. CASC7 and TP73 expression were significantly lower, whereas miR-34a-5p expression was higher in PTC tissues than the adjacent normal tissues. Furthermore, CASC7 overexpression inhibited cell proliferation and migration, whereas facilitated cell apoptosis in human PTC cell lines (K1 and TPC-1). Mechanistically, CASC7 acted as a sponge of miR-34a-5p to upregulate TP73 expression. Moreover, miR-34a-5p mimic transfection could abate the CASC7-regulated PTC cell proliferation, migration, and apoptosis. Collectively, CASC7 inhibited the proliferation and migration of PTC cells by sponging miR-34a-5p to upregulate TP73 expression.

Highlights

  • Thyroid cancer (TC) is the most common endocrine malignancy, accounting for about 1% of all human malignant neoplasms [1, 2]

  • cancer susceptibility candidate 7 (CASC7) overexpression inhibited papillary thyroid cancer (PTC) cell proliferation and migration, and induced PTC cell apoptosis Quantitative real-time PCR (qRT-PCR) analysis showed that CASC7 expression was significantly lower in most PTC tissues than that in adjacent normal tissues (Fig. 1a)

  • Transwell migration assay demonstrated that the number of migrated cells in PTC cells following CASC7 overexpression was notably less than that in those transfected with empty vector (Fig. 1e)

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Summary

Introduction

Thyroid cancer (TC) is the most common endocrine malignancy, accounting for about 1% of all human malignant neoplasms [1, 2]. PTC is the most prevalent form of thyroid malignancy, accounting for more than 80% of TC [4]. Considerable studies have confirmed that the abnormal expression of lncRNAs is closely related to the initiation and development of various cancers, including PTC [7, 8]. Certain lncRNAs are lowly expressed in PTC tissues and have tumor-suppressive function in PTC, for example, H19 [9], maternally expressed 3 [10], and BRAF-activated non-protein coding RNA [11]. Certain lncRNAs that are highly expressed in PTC tissues to exert oncogenic function in PTC, for example, copy number amplified long noncoding RNA in papillary thyroid cancer 1 [12], lncRNA-activated by TGF-beta [13], and nuclear paraspeckle assembly transcript 1 [14]

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