<p>LncRNA SNHG16 drives proliferation and invasion of papillary thyroid cancer through modulation of miR-497</p>

Abstract

BackgroundLong noncoding small nucleolar RNA host gene 16 (SNHG16) has been shown to play an oncogenic role in multiple cancers. However, the biological roles and mechanism of SNHG16 action in the regulation of papillary thyroid cancer (PTC) remains unknown. The aims of this study were to investigate the roles and the possible mechanism of SNHG16 in PTC progression.Materials and methodsThe expression of SNHG16 PTC tissues and cell lines was detected by reverse-transcription quantitative PCR (qRT-PCR). The effect of SNHG16 on cell proliferation, apoptosis, migration, and invasion was detected by Cell Counting Kit-8, flow cytometry, wound-healing assay, and Matrigel invasion assay, respectively. In addition, the regulatory relationships between SNHG16 and miR-497 were explored by luciferase reporter assay and qRT-PCR.ResultsThe SNHG16 expression was upregulated in PTC tissues and cell lines, whose expression was positively associated with advanced TNM stage and lymph node metastasis. Function analysis demonstrated that depletion of SNHG16 in PTC cells significantly inhibited cell proliferation, induced cell apoptosis, and suppressed cell migration and invasion abilities. Mechanistic studies indicated that SNHG16 functioned as an endogenous sponge for miR-497 to regulate its target genes brain-derived neurotrophic factor and yes-associated protein 1 expression. Furthermore, the inhibition of miR-497 antagonized the suppressive effect of SNHG16-depleted cells on cell proliferation, migration, and invasion.ConclusionThese findings revealed that SNHG16 drived the PTC progression possibly via regulating miR-497, suggesting that SNHG16 might be a novel therapeutic agent for PTC.

Long non‐coding RNA SNHG16 promotes proliferation and inhibits apoptosis of diffuse large B‐cell lymphoma cells by targeting miR‐497‐5p/PIM1 axis

“…However, the biological role of SNHG16 and its underlying mechanism in DLBCL are still unknown. SNHG16 acts as a molecular sponge for miR‐497‐5p to promote the proliferation and invasion of papillary thyroid cancer cells . miR‐497‐5p is underexpressed in human primary NPM‐ALK+ primary lymphoma and inhibits cell cycle progression in cancer cells .…”

“…SNHG16 acts as a molecular sponge for miR-497-5p to promote the proliferation and invasion of papillary thyroid cancer cells. 25 miR-497-5p is underexpressed in human primary NPM-ALK+ primary lymphoma and inhibits cell cycle progression in cancer cells. 26 Additionally, miR-497-5p functions as a tumour suppressor via targeting the Raf-1-mediated MAPK/ERK pathway in multiple myeloma cells.…”

<p><em>SNHG16</em>: A Novel Long-Non Coding RNA in Human Cancers</p>

“…41 Wen et al found that knockdown of SNHG16 inhibits migration and invasion of TPC-1 cells via regulating miR-497. 42 Interestingly, Vahid found a correlation between SNHG16 expression and the vitamin D receptor (VDR), which supports the hypothesis of an interactive network between SNHG16, VDR, and miR-98 in the context of cancer. 59 SNHG16 is expected to become a novel molecular marker for diagnosis, prognosis, and treatment of BC.…”

“…41 SNHG16 is upregulated in both papillary thyroid tissues and cell lines, which indicates advanced TNM stage and lymph node metastasis. 42 In addition to sequencing in tumor tissues, lncRNA levels can also be measured in exosomes. Exosomes, which are microvesicles (70-120 nm) derived from endosomes secreted by many cell types, can participate in intercellular communication by transferring intracellular substances (such as proteins, lipids, and nucleic acids, including lncRNA).…”

Identification of key miRNAs in papillary thyroid carcinoma based on data mining and bioinformatics methods

“…Papillary thyroid carcinoma (PTC) is the main histological type of thyroid cancer, accounting for >80% of all thyroid malignancies (1). Although most patients with PTC have low recurrence rate and exhibit optimal prognosis as determined by long term follow-up, approximately 15% of patients demonstrate aggressive behavior and poor outcome (2,3). To date, the pathogenesis of PTC has not been fully identified.…”