Circ_0000218 plays a carcinogenic role in laryngeal cancer through regulating microRNA-139-3p/Smad3 axis.

Laryngeal squamous cell carcinoma (LSCC) accounts for about 85%-90% of all cases of laryngeal cancer. So far, the role and molecular mechanism of circular RNA 0,000,218 (circ_0000218)/microRNA (miR)-139-3p in laryngeal cancer are not clear. The present study aimed to investigate the role and regulatory mechanism of circ_0000218/miR-139-3p in laryngeal cancerin vitro and in vivo. quantitative real time polymerase chain reaction (qRT-PCR) was used to detect the expression of circ_0000218/miR-139-3p in LSCC cells. Dual luciferase reporter assay and RNA immunoprecipitation (RIP) assay were used to confirm binding sites between miR-139-3p and smad family member 3 (Smad3), and circ_0000218 and miR-139-3p. Cell Counting Kit-8 (CCK-8) and cell apoptosis analysis were used to detect cell viability and apoptosis. Xenograft experiment was performed to show in vivo effect of circ_0000218/miR-139-3p on the growth of LSCC. Circ_0000218 was highly expressed in LSCC cells. miR-139-3p, lower expressed in LSCC cells, was negatively regulated by circ_0000218 in LSCC cells. Besides, the findings suggested that circ_0000218 silencing inhibited the LSCC cell viability and promoted apoptosis by negatively regulating miR-139-3p expression. Furthermore, the data indicated that miR-139-3p inhibited the viability of LSCC cells and promoted apoptosis, and these effects were reversed by Smad3 over-expression. In addition, the in vivo effects of circ_0000218/miR-139-3p on LSCC were consistent with the in vitro study. circ_0000218 inhibition inhibited the growth of LSCC by targeting miR-139-3p/Smad3 axis. Our present study provided a new target for laryngeal cancer treatment.

Bai Y ，Hou J ，Wang X ，Geng L ，Jia X ，Xiang L ，Nan K ... -  《-》

Circ_0023028 contributes to the progression of laryngeal squamous cell carcinoma by upregulating LASP1 through miR-486-3p.

Zheng Y ，Duan L ，Yang Y ，Luo D ，Yan B ... -  《-》

Circ_0044520 regulates the progression of laryngeal squamous cell carcinoma via the miR-338-3p/ROR2 axis.

Yang H ，Yu G ，Wang Y ，Guo X ... -  《-》

CircRNA CORO1C Regulates miR-654-3p/USP7 Axis to Mediate Laryngeal Squamous Cell Carcinoma Progression.

Circular RNAs have attracted the attention in the research on laryngeal squamous cell carcinoma (LSCC) development. But the function and mechanism of circRNA coronin-1C (circ_CORO1C) in LSCC progression are largely unknown. Circ_CORO1C, microRNA (miR)-654-3p, and ubiquitin-specific protease 7 (USP7) levels in LSCC tissues and cells were determined. Quantitative reverse transcription polymerase chain reaction and western blotting assays were conducted to determine the mRNA and protein levels of genes. Functional assays were further investigated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT), EdU staining, flow cytometry, transwell and xenograft assays. The binding relationship was examined by dual-luciferase reporter assay. Circ_CORO1C expression was elevated in LSCC samples and cells. circ_CORO1C silencing constrained cell proliferation and promoted apoptosis via reducing cell proliferation, inducing cell cycle arrest, inhibiting epithelial-mesenchymal transition, and promoting apoptosis, as well as restraining cell migration and invasion. USP7 is highly expressed in LSCC tissues and cells, and its expression was suppressed by circ_CORO1C silencing. Besides, the up-regulation of USP7 attenuated the influence of circ_CORO1C silencing on LSCC cell progression. Both circ_CORO1C and USP7 could bind to miR-654-3p. circ_CORO1C regulated USP7 expression by modulating miR-654-3p. miR-654-3p knockdown mitigated the influence of circ_CORO1C silence on LSCC cell progression. Furthermore, circ_CORO1C silencing reduced tumor growth in vivo. In conclusion, circ_CORO1C is highly expressed in LSCC tissues and cells, and circ_CORO1C silencing repressed LSCC progression via regulating miR-654-3p/USP7 axis.

Zhang J ，Li H ，Li J ，Ke S ... -  《-》

Circ_0120175 promotes laryngeal squamous cell carcinoma development through up-regulating SLC7A11 by sponging miR-330-3p.

The aim of our study was to illustrate the role of circular RNA 0120175 (circ_0120175) and its associated mechanism in laryngeal squamous cell carcinoma (LSCC) development. The abundance of circ_0120175, microRNA-330-3p (miR-330-3p) and solute carrier family 7, membrane 11 (SLC7A11) messenger RNA and protein was measured by quantitative real time polymerase chain reaction and Western blot assay. Cell proliferation, apoptosis, migration and invasion were assessed by cell counting kit-8 assay, flow cytometry and transwell migration and invasion assays, respectively. The interaction between miR-330-3p and circ_0120175 or SLC7A11 was confirmed by dual-luciferase reporter assay. Murine xenograft model was established to test the function of circ_0120175 in tumor growth in vivo. Circ_0120175 abundance was aberrantly increased in LSCC tissues and cell lines, and LSCC patients with high level of circ_0120175 were associated with advanced tumor staging, lymph node metastasis and short survival time. Circ_0120175 interference suppressed cell proliferation, migration and invasion and induced cell apoptosis of LSCC cells. Circ_0120175 could sponge and negatively regulate miR-330-3p expression in LSCC cells. The addition of anti-miR-330-3p partly reversed circ_0120175 knockdown-induced effects in LSCC cells. SLC7A11 bound to miR-330-3p. Circ_0120175 enhanced the abundance of SLC7A11 through sponging miR-330-3p in LSCC cells. Circ_0120175 silencing-mediated influences in LSCC cells were partly counteracted by the overexpression of SLC7A11. Circ_0120175 interference notably suppressed xenograft tumor growth in vivo. Circ_0120175 promoted proliferation, migration and invasion while impeded cell apoptosis of LSCC cells through miR-330-3p/SLC7A11 axis, which provided novel therapeutic targets for LSCC.

Fan D ，Zhu Y 《-》