Integrin α7 correlates with worse clinical features and prognosis, and its knockdown inhibits cell proliferation and stemness in tongue squamous cell carcinoma

Increasing evidence has displayed critical roles of circular RNAs (circRNAs) in tongue squamous cell carcinoma (TSCC). Hsa_circ_0043265 (circ_0043265) has been identified as a tumor suppressor in various tumors. Nevertheless, the critical roles of circ_0043265 in the initiation and progression of TSCC are yet to be fully elucidated. In our study, RNA and protein expressions were detected via qRT-PCR and Western blot. Cell proliferation, migration and invasion were evaluated via CCK-8 and transwell assays. The interactions between circ_0043265, miR-1243 and SALL1 were analyzed via bioinformatics analyses, RNA pull-down and luciferase assays, respectively. The current study demonstrated that circ_0043265 expression was downmodulated in TSCC tissues and cell lines (SCC25, SCC15, SCC9 and Cal27). Functionally, circ_0043265 overexpression led to an attenuation of cell proliferation, migration and invasion of SCC25 and Cal27 cells. Mechanistically, circ_0043265 acted as a competing endogenous RNA (ceRNA) via competitively sponging miR-1243, and restoration of miR-1243 rescued the inhibitory effects of circ_0043265 on cell proliferation, migration and invasion of SCC25 and Cal27 cells. Finally, it was observed that spalt like transcription factor 1 (SALL1), a potential target of miR-1243, was positively modulated via circ_0043265 in SCC25 and Cal27 cells, and SALL1 knockdown reversed the inhibitory effects of circ_0043265 on SCC25 and Cal27 cells. Collectively, the current study demonstrated that circ_0043265 was downmodulated in TSCC and was identified as a ceRNA that restrained the cell proliferation, migration and invasion of SCC25 and Cal27 cells via modulating the miR-1243/SALL1 axis.

Download Full-text

MicroRNA-149 targets specificity protein 1 to suppress human tongue squamous cell carcinoma cell proliferation and motility

Oncology Letters ◽

10.3892/ol.2016.5527 ◽

2016 ◽

Vol 13 (2) ◽

pp. 851-856 ◽

Cited By ~ 3

Author(s):

Jingxin Chen ◽

Jimin Chen ◽

Weizhong Li

Keyword(s):

Cell Proliferation ◽

Squamous Cell Carcinoma ◽

Cell Carcinoma ◽

Squamous Cell ◽

Carcinoma Cell ◽

Tongue Squamous Cell Carcinoma ◽

Squamous Cell Carcinoma Cell ◽

Specificity Protein 1 ◽

Human Tongue ◽

Specificity Protein

Download Full-text

Qilan Preparation Inhibits Proliferation and Induces Apoptosis by down-regulating microRNA-21 in Human Tca8113 Tongue Squamous Cell Carcinoma Cells

10.21203/rs.3.rs-344688/v1 ◽

2021 ◽

Author(s):

Jiamin Ding ◽

Zuoliang Chen ◽

Wanlu Chen ◽

Zhongxiong Ma ◽

Yunde Xie ◽

...

Keyword(s):

Cell Cycle ◽

Cell Proliferation ◽

Squamous Cell Carcinoma ◽

Cell Growth ◽

Cell Carcinoma ◽

Squamous Cell ◽

Tongue Squamous Cell Carcinoma ◽

Cell Counting ◽

Dependent Manner ◽

Pdcd4 Expression

Abstract Background: Qilan preparation, a complex Chinese herbal medicine consisting of ingredients extracted from Radix Astragali, Gynostemma Pentaphyllum, Rhizoma Chuanxiong and selenium- rich green tea and known for ‘fortifying the spleen and boosting qi, quickening the blood and transforming stasis, and resolving toxins and relieving pain, is used for the prevention and management of oral diseases. The aim of this study was to examine the antitumor effects of Qilan preparation on oral squamous cell carcinoma (OSCC) in vitro and to explore its underlying mechanisms of action. Methods: Human Tca8113 tongue squamous cell carcinoma (TSCC) cells were tested. Cell proliferation, cell cycle distribution and apoptosis were examined using cell counting kit-8 (CCK8) and flow cytometry (FCM). The expression of PTEN and PDCD4 were determined by western blot. Changes in miR-21 levels were quantified using TaqMan stem-loop real-time PCR. After miR-21 was transiently transfected into Tca8113 cells using Lipofectamine®3000, cell proliferation, apoptosis and miR-21 and PDCD4 expression levels were measured.Results: Qilan preparation inhibited Tca8113 cell growth in a dose- and time-dependent manner by inducing apoptosis and cell cycle arrest in S-phase, decreasing miR-21 levels and increasing PTEN and PDCD4 expression. MiR-21 overexpression reversed the Qilan preparation-induced suppression of cell proliferation and induction of apoptosis while also blocking the increase in PDCD4.Conclusions: Our study revealed, for the first time, the ability of Qilan preparation to suppress TSCC cell growth and elucidated that Qilan preparation elicits its anti-cancer actions via either the miR-21/PDCD4 or PTEN pathway.

Download Full-text

LncRNA CASC9 Affects Cell Proliferation, Migration, and Invasion of Tongue Squamous cell Carcinoma via Regulating miR-423-5p/SOX12 Axes

Cancer Management and Research ◽

10.2147/cmar.s220351 ◽

2020 ◽

Vol Volume 12 ◽

pp. 277-287 ◽

Cited By ~ 4

Author(s):

Xin Chen ◽

Hanfeng Xu ◽

Guowen Sun ◽

Ying Zhang

Keyword(s):

Cell Proliferation ◽

Squamous Cell Carcinoma ◽

Cell Carcinoma ◽

Squamous Cell ◽

Tongue Squamous Cell Carcinoma ◽

Migration And Invasion

Download Full-text

MicroRNA-7 targets IGF1R (insulin-like growth factor 1 receptor) in tongue squamous cell carcinoma cells

Biochemical Journal ◽

10.1042/bj20100859 ◽

2010 ◽

Vol 432 (1) ◽

pp. 199-207 ◽

Cited By ~ 148

Author(s):

Lu Jiang ◽

Xiqiang Liu ◽

Zujian Chen ◽

Yi Jin ◽

Caroline E. Heidbreder ◽

...

Keyword(s):

Cell Proliferation ◽

Squamous Cell Carcinoma ◽

Growth Factor ◽

Cell Carcinoma ◽

Squamous Cell ◽

Tongue Squamous Cell Carcinoma ◽

Luciferase Reporter ◽

Insulin Like Growth Factor ◽

Luciferase Reporter Gene ◽

Igf1r Expression

miR-7 (microRNA-7) has been characterized as a tumour suppressor in several human cancers. It targets a number of proto-oncogenes that contribute to cell proliferation and survival. However, the mechanism(s) by which miR-7 suppresses tumorigenesis in TSCC (tongue squamous cell carcinoma) is unknown. The present bioinformatics analysis revealed that IGF1R (insulin-like growth factor 1 receptor) mRNA is a potential target for miR-7. Ectopic transfection of miR-7 led to a significant reduction in IGF1R at both the mRNA and protein levels in TSCC cells. Knockdown of miR-7 in TSCC cells enhanced IGF1R expression. Direct targeting of miR-7 to three candidate binding sequences located in the 3′-untranslated region of IGF1R mRNA was confirmed using luciferase-reporter-gene assays. The miR-7mediated down-regulation of IGF1R expression attenuated the IGF1 (insulin-like growth factor 1)-induced activation of Akt (protein kinase B) in TSCC cell lines, which in turn resulted in a reduction in cell proliferation and cell-cycle arrest, and an enhanced apoptotic rate. Taken together, the present results demonstrated that miR-7 regulates the IGF1R/Akt signalling pathway by post-transcriptional regulation of IGF1R. Our results indicate that miR-7 plays an important role in TSCC and may serve as a novel therapeutic target for TSCC patients.

Download Full-text