Long non-coding RNA CASC15 promotes tongue squamous carcinoma progression through targeting miR-33a-5p

Zuo, Zhibin; Ma, Long; Gong, Zuode; Xue, Lixiang; Wang, Qibao

doi:10.1007/s11356-018-2300-z

Cited by 25 publications

(15 citation statements)

References 36 publications

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“…Future studies may also focus on the mechanism of the actions of CASC15 in TSCC. It is worth noting that Zuo et al in a recent study investigated the role of CASC15 in TSCC and they found that CASC15 can target miR-33a-5p to regulate the migration of TSCC cells [18], which is consistent with the data of our studies. However this study also showed that CASC15 overexpression resulted in the accelerated proliferation of TSCC cells, which is inconsistent with our study.…”

Section: Discussionsupporting

confidence: 92%

LncRNA CACS15 regulates tongue squamous cell carcinoma cell behaviors and predicts survival

Chen

et al. 2019

BMC Oral Health

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BackgroundThe involvement of lncRNA CASC15 in several types of cancers has been reported, while its role in tongue squamous cell carcinoma (TSCC) is unknown. Our study aimed to investigate the clinical potentials of lncRNA CASC15 in TSCC.MethodsThe expression of CASC15 and miR-124 in tissue samples from TSCC patients and TSCC cell lines was analyzed by qPCR. Overexpression experiments were performed to analyze the interactions between CASC15 and miR-124. Survival analysis was performed to analyze the prognostic values of CASC15 and miR-124 for TSCC. Transwell assays were performed to analyze cell invasion and migration.ResultsWe found that CASC15 was upregulated, while miR-124 was downregulated in TSCC tissues than in non-cancer tissues of TSCC patients. CASC15 and miR-125 expression was not significantly different among patients with different clinical stages, and patients with high level of CASC15 and low level of miR-125 showed low overall survival rate. CASC15 and miR-124 were inversely correlated in TSCC tissues, and CASC15 overexpression in TSCC cells resulted in downregulation of miR-124. In contrast, overexpression of miR-124 showed no significant effect on CASC15 expression. CASC15 overexpression resulted in the increased, while miR-124 overexpression resulted in the decreased migration and invasion rates of TSCC cells.ConclusionCASC15 and miR-124 predict TSCC patients’ survival and CASC15 may downregulate miR-124 to inhibit TSCC cell migration and invasion.The study was approved by Ethics Committee of The first Affiliated Hospital of Jinzhou Medical University (20103548FAHJMU).

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Section: Discussionsupporting

confidence: 92%

LncRNA CACS15 regulates tongue squamous cell carcinoma cell behaviors and predicts survival

Chen

et al. 2019

BMC Oral Health

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“…For example, in osteosarcoma, overexpression of lncRNA DANCR inhibits the expression of miR-33a-5p; 21 and in tongue squamous carcinoma, lncRNA CASC15 targetedly inhibits miR-33a-5p. 22 However, the interaction between EGOT and miR-33a-5p has not been elucidated.…”

Section: Introductionmentioning

confidence: 99%

<p>Long Non-Coding RNA EGOT Promotes the Malignant Phenotypes of Hepatocellular Carcinoma Cells and Increases the Expression of HMGA2 via Down-Regulating miR-33a-5p</p>

Wu¹,

Ai²,

Zhang³

et al. 2019

OTT

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Background: Chronic hepatitis C virus (HCV) infection is an important risk factor for hepatocellular carcinoma (HCC). EGOT is a long non-coding RNA (lncRNA) induced after HCV infection that increases viral replication by antagonizing the antiviral response. Interestingly, EGOTalso acts as a crucial regulator in multiple cancers. However, its role in HCC remains unclear. Methods: Real-time PCR (RT-PCR) was used to detect the expression of EGOT in HCC samples and cell lines. CCK-8 assay and colony formation assay were performed to evaluate the effect of EGOT on proliferation. Scratch healing assay and transwell assay were used to detect the changes of migration and invasion. Flow cytometry was used to detect the effect of EGOT on apoptosis. Interaction between EGOT and miR-33a-5p was determined by bioinformatics analysis, RT-PCR, and dual-luciferase reporter assay. Western blot was used to confirm that high mobility group protein A2 (HMGA2) could be modulated by EGOT. Results: Compared with normal liver tissues, the expression level of EGOT in HCC tissues was significantly up-regulated. EGOT markedly regulated viability, migration and invasion of HCC cells. The expression level of EGOT was negatively correlated the expression level of miR-33a-5p. It is also confirmed that EGOT could specifically bind to miR-33a-5p and could reduce its expression, in turn, up-regulate the expression of HMGA2. Conclusion: Our data imply that EGOT may be a novel therapeutic target for HCC, and highlights the key role of EGOT/miR-33a-5p/HMGA2 in the progression of this deadly disease.

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“…Zuo et al (81) have reported that lncRNA CASC15 downregulates miR-33a-5p by miRNA sponging, thereby upregulating the miR-33a-5p target ZEB1 and enhancing the proliferation, migration and cell cycle of TSCC cells (Fig. 5B).…”

Section: Tongue Squamous Carcinoma (Tscc)mentioning

confidence: 97%

Role of microRNA‑33a in malignant cells (Review)

et al. 2020

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Cancer causes most of the mortality and morbidity worldwide, with a significant increase in incidence during recent years. MicroRNAs (miRNAs/miRs) are non-coding small RNAs capable of regulating gene expression. They regulate crucial cellular processes, including proliferation, differentiation, metastasis and apoptosis. Therefore, abnormal miRNA expression is associated with multiple diseases, including cancer. There are two types of cancer-associated miRNAs, oncogenic and tumor suppressor miRNAs, depending on their roles and expression patterns in cancer. Accordingly, miRNAs are considered to be targets for cancer prevention and treatment. miR-33a controls cellular cholesterol uptake and synthesis, which are both closely associated with carcinogenesis. The present review thoroughly describes the roles of miR-33a in more than a dozen types of cancer and the underlying mechanisms. Accordingly, the present review may serve as a guide for researchers studying the involvement of miR-33a in diverse cancer settings. Contents 1. Introduction 2. miR-33a and its role in cancer 3. Discussion 4. Conclusions

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Long non-coding RNA CASC15 promotes tongue squamous carcinoma progression through targeting miR-33a-5p

Cited by 25 publications

References 36 publications

LncRNA CACS15 regulates tongue squamous cell carcinoma cell behaviors and predicts survival

LncRNA CACS15 regulates tongue squamous cell carcinoma cell behaviors and predicts survival

<p>Long Non-Coding RNA EGOT Promotes the Malignant Phenotypes of Hepatocellular Carcinoma Cells and Increases the Expression of HMGA2 via Down-Regulating miR-33a-5p</p>

Role of microRNA‑33a in malignant cells (Review)

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