Abstract
Thyroid cancer (TC) is an endocrine malignancy with rising incidence. Long non-coding RNAs (lncRNAs) can serve as diagnostic and prognostic biomarkers for TC. Thus, we studied roles of LINC01296 in TC progression. Initially, the Gene Expression Omnibus (GEO) database was used to detect the differentially expressed genes in human TC samples and the potential mechanism. Expression of LINC01296 and miR-143-3p in TC tissues and cells was measured. The transfection of TC cells was conducted with si-LINC01296, si-Musashi 2 (MSI2), mimic or inhibitor of miR-143-3p to determine their effects on TC cell proliferation, migration, invasion, apoptosis and the AKT/STAT3 signaling pathway. Finally, in vivo assay was performed to verify role of miR-143-3p in tumorigenesis of TC cells in nude mice. LINC01296 was predicted to bind to miR-143-3p to modulate MSI2 expression, thus regulating the occurrence and development of TC. LINC01296 was up-regulated, while miR-143-3p was down-regulated in TC cells and tissues. LNC01296 specifically bound to miR-143-3p and MSI2 was a target of miR-143-3p. Besides, LINC01296 silencing or miR-143-3p overexpression inhibited migration, invasion, proliferation and advanced apoptosis of TC cells. Additionally, silenced LINC01296 or overexpressed miR-143-3p reduced phosphorylated STAT3/STAT3, phosphorylated AKT/AKT, B-cell lymphoma-2 (Bcl-2) and CyclinD1 levels but elevated BCL2-associated X (Bax), Cleaved Caspase3 and Caspase3 levels. Also, tumorigenesis of TC cells in nude mice was inhibited with the silencing of LINC01296. In summary, LINC01296/miR-143-3p/MSI2 axis regulated development of TC through the AKT/STAT3 signaling pathway.
Highlights
Thyroid cancer (TC) is the most prevalent cancer in the endocrine system and the incidence of TC has increased in women in the past 3 years worldwide, especially in the developed countries [1,2]
We demonstrated that the role of miR-143-3p and Musashi 2 (MSI2) in the cell proliferation, migration, invasion and apoptosis might depend on their regulation of the AKT/STAT3 signaling pathway
We considered that miR-143-3p was extremely critical, and through the Gene Expression Omnibus (GEO) database, significantly low expression of miR-143-3p was identified in TC (Figure 1C)
Summary
Thyroid cancer (TC) is the most prevalent cancer in the endocrine system and the incidence of TC has increased in women in the past 3 years worldwide, especially in the developed countries [1,2]. The major histological types of TC include follicular thyroid carcinoma (FTC), papillary thyroid carcinoma (PTC), and anaplastic thyroid carcinoma (UTC), among which PTC is the predominant one, followed by FTC [3]. The metastasis of TC could impair the lung and bone, which is closely correlated to high mortality [4]. Mortality caused by TC is rising in more advanced tumors [5]. TC can be treated through radioiodine therapy, the majority of patients with TC cannot be fully cured [6]. It is an urgent need to seek new insights into the treatment of TC
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