CircRNA CircRIMS is Overexpressed in Esophageal Squamous Cell Carcinoma and Downregulate miR-613 through Methylation to Increase Cell Proliferation

2020 ◽  
Author(s):  
Haijun Wan ◽  
Bosi Yuan ◽  
Kang Jiang ◽  
Juan Wei ◽  
Xiaoyue Feng ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Prognostic Value ◽  
Proliferation Assay ◽  
Inhibitory Effects ◽  
Poor Survival ◽  
Brdu Assay

Abstract BackgroundEsophageal squamous cell carcinoma (ESCC) as the most common subtype of esophageal cancer accounts for about 95% of all cases. CircRNA CircRIMS has been characterized as an oncogenic circRNA in gastric cancer, while its role in other cancers is unknown. This study aimed to explore the role of CircRIMS in esophageal squamous cell carcinoma (ESCC). MethodsTissues collected from 60 ESCC patients were used in this study. The expression of CircRIMS and miR-613 were detected by RT-qPCRs. The 60 ESCC patients were followed up for 5 years to evaluate the prognostic value of CircRIMS for ESCC. The role of CircRIMS in regulating the expression of miR-613 and methylation was assess by overexpression experiments and RT-qPCRs. The role of CircRIMS and miR-613 in regulating cell proliferation was analyzed by BrdU assay. ResultsWe found that CircRIMS was overexpressed in ESCC and predicted poor survival. In addition, miR-613 was downregulated in ESCC and inversely correlated with CircRIMS. In ESCC cells, overexpression of CircRIMS decreased the expression levels of miR-613 and increased the methylation of miR-613 gene. Cell proliferation assay showed that overexpression of CircRIMS reduced the inhibitory effects of overexpression of miR-613 on cell proliferation. ConclusionsCircRIMS may downregulate miR-613 through methylation to increase cell proliferation in ESCC.

PS02.201: EXPRESSION AND ROLE OF CLIC1 IN HUMAN ESOPHAGEAL SQUAMOUS CELL CARCINOMA

2018 ◽  
Vol 31 (Supplement_1) ◽  
pp. 179-179
Author(s):  
Toshiyuki Kobayashi ◽  
Atsushi Shiozaki ◽  
Hitoshi Fujiwara ◽  
Hirotaka Konishi ◽  
Yoshito Nako ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Microarray Analysis ◽  
Squamous Cell ◽  
Migration And Invasion ◽  
Poor Prognostic Factor ◽  
Weak Expression

Abstract Background Recent studies have reported important roles for chloride intracellular channel 1 (CLIC1) in various cancers; however, its involvement in esophageal squamous cell carcinoma (ESCC) remains unclear. The aim of the present study was to investigate the role of CLIC1 in human ESCC. Methods CLIC1 expression in human ESCC cell lines was analyzed by Western blotting. Knockdown experiments were conducted with CLIC1 siRNA, and their effects on cell proliferation, the cell cycle, apoptosis, migration, and invasion were analyzed. The gene expression profiles of cells were analyzed using a microarray analysis. An immunohistochemical analysis was performed on 61 primary tumor samples obtained from ESCC patients who underwent esophagectomy. Results ESCC cells strongly expressed CLIC1. The depletion of CLIC1 using siRNA inhibited cell proliferation, induced apoptosis, and promoted cell migration and invasion. The results of the microarray analysis revealed that the depletion of CLIC1 regulated apoptosis via the TLR2/JNK pathway. Immunohistochemistry showed that CLIC1 was present in the cytoplasm of carcinoma cells, and that the very strong or very weak expression of CLIC1 was an independent poor prognostic factor. Conclusion The present results suggest that the very strong expression of CLIC1 enhances tumor survival, while its very weak expression promotes cellular movement. The present study provides an insight into the role of CLIC1 as a switch among tumor behaviors in ESCC. Disclosure All authors have declared no conflicts of interest.

scholarly journals Hsa_circ_0043265 Restrains Cell Proliferation, Migration and Invasion of Tongue Squamous Cell Carcinoma via Targeting the miR-1243/SALL1 Axis

2021 ◽  
Vol 27 ◽  
Author(s):  
Cuijuan Qian ◽  
Yisheng Yang ◽  
Tianchen Lan ◽  
Yichao Wang ◽  
Jun Yao
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Tongue Squamous Cell Carcinoma ◽  
Migration And Invasion ◽  
Circular Rnas ◽  
Inhibitory Effects ◽  
Bioinformatics Analyses ◽  
Transcription Factor 1

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.

scholarly journals Prognostic Value of Combined Analysis of CTLA-4 and PLR in Esophageal Squamous Cell Carcinoma (ESCC) Patients

2019 ◽  
Vol 2019 ◽  
pp. 1-7
Author(s):  
Cui-Ying Zhang ◽  
Juan Zhang ◽  
Yun-Fan Ma ◽  
Hong Zhe ◽  
Ren Zhao ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Prognostic Value ◽  
Cytotoxic T Lymphocyte ◽  
Expression Level ◽  
Prognostic Role ◽  
Combined Analysis

Objective. The purpose of this study was to evaluate the prognostic role of the cytotoxic T-lymphocyte-associated antigen-4 (CTLA-4) expression level and the platelet lymphocyte ratio (PLR) level in esophageal squamous cell carcinoma (ESCC) patients. Methods. 84 ESCC patients who received surgical treatment in our hospital were enrolled in the study. The correlation of each biomarker’s level with ESCC patients’ clinicopathological characteristics and overall survival (OS) was assessed. Results. The elevated expression rate of T-CTLA-4 (tumor cell CTLA-4) and I-CTLA-4 (interstitial lymphocyte CTLA-4) was 48.8% and 44.0%, respectively. The number of enrolled patients with a higher PLR level (≥119) was 48. The prognostic value of T-CTLA-4, I-CTLA-4, and PLR in ESCC patients was not detected. However, patients with both a low T-CTLA-4 expression level and a low PLR level that had longer OS (p=0.023) were found. The prognostic role of T-CTLA-4(-) +PLR (-) status in ESCC patients was also confirmed in multivariate analyses (p=0.027). Conclusion. These results demonstrated the potential prognostic value of combined analysis of CTLA-4 and PLR in ESCC patients.

scholarly journals IQGAP1 silencing suppresses the malignant characteristics of laryngeal squamous cell carcinoma cells

2017 ◽  
Vol 33 (1) ◽  
pp. 73-78 ◽  
Author(s):  
Xiaoxia Wang ◽  
Chun He ◽  
Chaohui Li ◽  
Benhong Ren ◽  
Qing Deng ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Epithelial To Mesenchymal Transition ◽  
Laryngeal Squamous Cell Carcinoma ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
First Time

Background: Laryngeal squamous cell carcinoma (LSCC) has a poor prognosis due to recurrence and metastasis. IQ-domain GTPase-activating protein 1 (IQGAP1), a scaffold protein, plays an important role in tumorigenesis and malignant development. In this study, we aimed to explore the role of IQGAP1 in LSCC. Methods: Expression of IQGAP1 in human LSCC specimens was assessed by immunohistochemistry. We also evaluated the roles of IQGAP1 in cell proliferation, migration and invasion and epithelial-to-mesenchymal transition (EMT) in Hep-2 cells. Results: The expression of IQGAP1 protein was significantly up-regulated in LSCC tissues compared with normal laryngeal tissues (p = 0.002). Furthermore, the knockdown of IQGAP1 in Hep-2 cells inhibited cell growth, migration and invasion. Moreover, we found that IQGAP1 silencing reversed EMT. Conclusions: These results show for the first time that IQGAP1 is up-regulated in LSCC tissues and plays an important role in LSCC cell proliferation and invasiveness, which indicates that IQGAP1 could work as an oncogene and may serve as a promising molecular target for treatment of LSCC.

scholarly journals Prognosis and functional role of EIF4G1 in lung squamous cell carcinoma

2021 ◽  
Author(s):  
Baoxin Bai ◽  
Lingwei Wang ◽  
Zhiyuan Huang ◽  
Zhiwen Zhang ◽  
Ying Lu ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Functional Role ◽  
Lung Squamous Cell Carcinoma ◽  
High Expression ◽  
Expression Levels

Abstract Purpose To study the functional role and prognosis of EIF4G1 in lung squamous cell carcinoma (LSCC). Methods The clinical relevance of EIF4G1 in LSCC was investigated following detection of the expression levels of EIF4G1 by immunohistochemical staining (IHC). The expression levels of EIF4G1, AKT2, p-AKT, mTOR, cyclin D1 and β-actin were detected by western blot analysis. The cell proliferation and colony formation assays were used to detect the cell proliferative ability; flow-cytometry was used to assess the cell cycle; an invasion assay was used to detect cell invasive ability and the real-time quantitative polymerase chain reaction (Q-PCR) assay was used to assess the expression levels of EIF4G1 and β-actin. The role of EIF4G1 was verified by xenograft models. These experimental methods were employed to assess the functional role of EIF4G1 in LSCC pathogenesis. Results EIF4G1 was overexpressed in LSCC tumor tissues (P < 0.05) compared with the corresponding expression noted in paired adjacent tissues and cells. The expression levels of EIF4G1 were dependent on age (P = 0.002) and clinical stage (I vs II vs III + IV) (P < 0.001). High expression of EIF4G1 (P = 0.008, HR = 2.277, 95% CI = 1.250–4.145) could be used to predict the overall survival of LSCC patients as determined by the Cox’s proportional hazard model. High expression of EIF4G1 exhibited a lower survival (LogRank = 7.167, P = 0.007) in LSCC. Downregulation of EIF4G1 significantly inhibited LSCC proliferation, invasion and cell cycle progression. Conclusion EIF4G1 promotes LSCC cell proliferation and may represent an indicator of prognosis in LSCC.

scholarly journals LncRNA SLC7A11-AS1 is Upregulated in Colorectal Cancer and Promotes the Proliferation of Cancer Cells by Suppressing the Maturation of miR-34a

2021 ◽  
Author(s):  
Peijiang Chang ◽  
Maosheng Wang
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cancer Biology ◽  
Prognostic Value ◽  
Inhibitory Effects ◽  
Poor Survival ◽  
Tumor Tissues ◽  
Tcga Dataset

Abstract Background: LncRNA SLC7A11-AS1 is recently characterized critical player in cancer biology. We analyzed TCGA dataset and observed the upregulation of SLC7A11-AS1 in colorectal cancer (CRC). We therefore analyzed the role of SLC7A11-AS1 in CRC. Methods: Paired CRC and non-tumor tissues were collected from 60 CRC patients and expression of SLC7A11-AS1 in tissues was determined by RT-qPCR. The 60 CRC patients were followed up for 5 years to analyze the prognostic value of SLC7A11-AS1 for CRC. Correlations were analyzed by linear regression. The effects of SLC7A11-AS1 overexpression on the expression of miR-34a precursor and mature miR-34a were analyzed by RT-qPCR. Cell proliferation was analyzed by CCK-8 assay.Result: SLC7A11-AS1 was upregulated in CRC and predicted poor survival. SLC7A11-AS1 and mature miR-34a were inversely correlated, while SLC7A11-AS1 was not significantly correlated with the precursor of miR-34a. In CRC cells, SLC7A11-AS1 overexpression resulted in the reduced level of mature miR-34a, but not miR-34a precursor. Moreover, SLC7A11-AS1 overexpression reduced the inhibitory effects of miR-34a overexpression on cell proliferation. Conclusion: SLC7A11-AS1 may promote the proliferation of cancer cells in CRC by suppressing the maturation of miR-34a.

scholarly journals LncRNA HOXA-AS2 promotes tumor progression via suppressing miR- 567 expression in Oral Squamous Cell Carcinoma 

2021 ◽  
Author(s):  
Rui Chen ◽  
Xi Wang ◽  
Shixian Zhou ◽  
Zongyue Zeng
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Biological Function ◽  
Human Cancer ◽  
Direct Interaction ◽  
Poor Survival ◽  
Non Coding Rnas

Abstract Growing evidence shows that long non-coding RNAs (lncRNAs), such as lncRNA HOXA-AS2, have emerged as critical regulators in human cancer. However, the biological function and detail regulating mechanisms that how lncRNA HOXA-AS2 played in oral squamous cell carcinoma (OSCC) remains unexplored. In this study, high expression of lncRNA HOXA-AS2 was determined in OSCC cell lines and clinical tissues, which positively correlated with advanced TNM stage and poor survival of OSCC patients. In mechanism, we found that lncRNA HOXA-AS2 negatively regulated miR-567 expression by direct interaction. Additionally, we also found that the expression of miR-567 inversely decreased in OSCC tissues along with the up-regulation of lncRNA HOXA-AS2. Functionally, overexpression of lncRNA HOXA-AS2 significantly promoted OSCC cell proliferation, while knockdown of lncRNA HOXA-AS2 significantly inhibited it. Additionally, we determined that miR-567 targeted to CDK8 directly at the 3’ UTR. In conclusion, lncRNA HOXA-AS2 was up-rugulated in OSCC, correlated with poor clinical outcomes, and promoted OSCC cell proliferation via sponging miR-567 to promote CDK8 expression. Therefore, the potential prognostic value of lncRNA HOXA-AS2 could be explored further.

scholarly journals Upregulation of far upstream element-binding protein 1 (FUBP1) promotes tumor proliferation and unfavorable prognosis in tongue squamous cell carcinoma

2020 ◽  
Vol 35 (2) ◽  
pp. 56-65
Author(s):  
Yang Chen ◽  
Jiameng Liu ◽  
Ningbo Geng ◽  
Chongjin Feng
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Western Blot ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Poor Prognosis ◽  
Qrt Pcr ◽  
Upstream Element

Background: A well-known transcriptional regulator of the proto-oncogene c-Myc, far-upstream element (FUSE) binding protein 1 (FUBP1) has been demonstrated by previous work to be aberrantly expressed in lots of cancers and plays a critical role in tumor progression; however, its expression and function in tongue squamous cell carcinoma (TSCC) remains unclear. Methods: Evaluations with immunohistochemistry, quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot were performed to assess FUBP1 expression. The correlations of FUBP1 expression levels with various clinicopathological factors were evaluated with univariate and multivariate analyses. In addition, the role of FUBP1 in TSCC proliferation was studied in TSCC cells by silencing FUBP1. The role of FUBP1 on proliferation and apoptosis was confirmed by cell counting Kit-8, colony formation, cell cycle, and cell apoptosis assays. Results: Immunohistochemistry, qRT-PCR and Western blot results showed FUBP1 expression was higher in TSCC tissues in comparison with adjacent non-cancerous tissues ( P <0.05), as well as in patients with advanced-stage disease or cervical lymph node metastasis ( P<0.001). The 5-year survival rate was significantly lower in the group with high FUBP1 expression than in that with low FUBP1 expression ( P=0.035). FUBP1 expression was also an independent predictor for overall survival in TSCC patients, and was closely related to poor prognosis. FUBP1 knockdown inhibited cancer cell proliferation, and induced cell cycle arrest and apoptosis. Conclusion: FUBP1 was overexpressed in TSCC, and correlated with TSCC cell proliferation and poor prognosis. FUBP1 appears to act as a potential oncogene in TSCC, and may be considered a novel biomarker for TSCC.

scholarly journals Oncogenic role of MiR-130a in oral squamous cell carcinoma

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Karthik Mallela ◽  
Swamy Shivananda ◽  
Kodaganur S. Gopinath ◽  
Arun Kumar
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Therapeutic Strategy ◽  
Inverse Correlation ◽  
Migration And Invasion ◽  
Cellular Functions

AbstractAberrant activation of the PI3K/AKT/mTOR pathway is attributed to the pathogenesis of oral squamous cell carcinoma (OSCC). In recent years, increasing evidence suggests the involvement of microRNAs (miRNAs) in oral carcinogenesis by acting as tumor suppressors or oncogenes. TSC1, as a component of the above pathway, regulates several cellular functions such as cell proliferation, apoptosis, migration and invasion. Downregulation of TSC1 is reported in oral as well as several other cancers and is associated with an unfavourable clinical outcome in patients. Here we show that oncogenic miR-130a binds to the 3′UTR of TSC1 and represses its expression. MiR-130a-mediated repression of TSC1 increases cell proliferation, anchorage independent growth and invasion of OSCC cells, which is dependent on the presence of the 3′UTR in TSC1. We observe an inverse correlation between the expression levels of miR-130a and TSC1 in OSCC samples, suggesting that their interaction is physiologically relevant. Delivery of antagomiR-130a to OSCC cells results in a significant decrease in xenograft size. Taken together, the findings of the study indicate that miR-130a-mediated TSC1 downregulation is not only a novel mechanism in OSCC, but also the restoration of TSC1 levels by antagomiR-130a may be a potential therapeutic strategy for the treatment of OSCC.

Sign in / Sign up

Export Citation Format

Share Document