MicroRNA-33a-5p suppresses esophageal squamous cell carcinoma progression via regulation of lncRNA DANCR and ZEB1

Zhang, Chunyan; Wang, Lingxu; Yang, Juanjuan; Yin, Fang‐Fang; Li, Hongzhi; Xie, Linsen; Cui, Yuanbo

doi:10.1016/j.ejphar.2019.172590

Cited by 27 publications

(17 citation statements)

References 21 publications

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“…[13][14][15] LncRNAs play an important part during ESCC initiation and progression by performing either oncogenic or tumor-suppressive functions. [16][17][18] These observations have collectively uncovered the crucial regulatory role of lncRNAs in the pathogenesis of ESCC, suggesting that lncRNAs might be promising targets for the diagnosis, prognosis, prevention, and treatment of ESCC.…”

Section: Introductionmentioning

confidence: 93%

Long Noncoding RNA FGD5-AS1 Acts as a Competing Endogenous RNA on microRNA-383 to Enhance the Malignant Characteristics of Esophageal Squamous Cell Carcinoma by Increasing SP1 Expression

Jia

Zhang

Hong

et al. 2020

CMAR

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These authors contributed equally to this workPurpose: Previous studies have identified the important roles of a long noncoding RNA called FGD5 antisense RNA 1 (FGD5-AS1) in several types of human cancer. Nonetheless, to our knowledge, the expression and functions of FGD5-AS1 in esophageal squamous cell carcinoma (ESCC) have not been clarified. In this study, we aimed to determine the expression status of long noncoding RNA FGD5-AS1 in ESCC, determine its participation in ESCC progression, and uncover the underlying mechanisms. Methods: ESCC tissue samples and paired normal adjacent tissues were collected to quantify FGD5-AS1 expression by reverse-transcription quantitative PCR. The effects of FGD5-AS1 on ESCC cell proliferation, apoptosis, migration, and invasion in vitro as well as tumor growth in vivo were studied using a Cell Counting Kit-8 assay, flow cytometry, Transwell migration and invasion assays, and an in vivo tumor xenograft experiment. Results: FGD5-AS1 was found to be aberrantly upregulated in both ESCC tumors and cell lines compared to the control groups. Increased FGD5-AS1 expression manifested a close association with tumor size, TNM stage, and lymph node metastasis in patients with ESCC. Overall survival of patients with ESCC was shorter in the FGD5-AS1 high-expression group than in the FGD5-AS1 low-expression group. An FGD5-AS1 knockdown markedly attenuated ESCC cell proliferation, migration, and invasion and promoted apoptosis in vitro as well as slowed tumor growth in vivo. Mechanism investigation revealed that FGD5-AS1 can increase SP1 expression by sponging microRNA-383 (miR-383), thus functioning as a competing endogenous RNA. An miR-383 knockdown and recovery of SP1 expression attenuated the inhibition of the malignant characteristics of ESCC cells by the FGD5-AS1 knockdown. Conclusion: Thus, FGD5-AS1 enhances the aggressive phenotype of ESCC cells in vitro and in vivo via the miR-383-SP1 axis, which may represent a novel target for ESCC therapy.

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Section: Introductionmentioning

confidence: 93%

Long Noncoding RNA FGD5-AS1 Acts as a Competing Endogenous RNA on microRNA-383 to Enhance the Malignant Characteristics of Esophageal Squamous Cell Carcinoma by Increasing SP1 Expression

Jia

Zhang

Hong

et al. 2020

CMAR

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“…It targets and downregulates ZEB1 and thereby suppresses ESCC proliferation and migration ( Fig. 3D) (62). Notably, lncRNA differentiation antagonizing non-protein coding RNA (DANCR) downregulates miR-33a-5p levels through miRNA sponging in ESCC (62).…”

Section: Mir-33a and Its Role In Cancermentioning

confidence: 99%

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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“…Numerous miRNAs were revealed to be dysregulated in various of human tumors, and a part of these dysregulated miRNAs have already been demonstrated to be involved in the pathological conditions in tumor cell [13]. Currently, the implication of miRNAs in ESCC have also been well documented by numerous studies, where more and more ESCC-related miRNAs have been identified, such as miR-27a, miR-33a-5p, miR-134, and miR-4324 [14][15][16][17]. Nevertheless, the entire regulatory network of miRNAs in ESCC still remains unknown.…”

Section: Introductionmentioning

confidence: 99%

PIK3C3 Acts as a Tumor Suppressor in Esophageal Squamous Cell Carcinoma and Was Regulated by MiR-340-5p

Wang

et al. 2020

Med Sci Monit

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Background: Esophageal squamous cell carcinoma (ESCC), a major histological subtype of esophageal cancer, is a common cause of tumor-related deaths in the world. Due to the lack of understanding of the pathogenesis of ESCC, its clinical treatment is still a big challenge. In the present study, we aimed to identify an ESCC-related gene in the GEO dataset, and to explore its function and mechanism in ESCC. Material/Methods: The GSE dataset (GSE100492) consisting of 10 samples was analyzed using GEO2R for identifying the differentially expressed genes between ESCC and normal samples. Expression levels of mRNA and miRNA in ESCC tissues and cells were detected via quantitative real-time polymerase chain reaction. Protein expression was analyzed by western blot. Cell proliferation viability was determined through MTT and colony formation. Cell distribution and apoptosis was detected by flow cytometry. MiRNA target prediction was analyzed by bioinformatics. The interplay between miR-340-5p and PIK3C3 was validated by dual-luciferase reporter assay. Results: PIK3C3 was lowly expressed in ESCC tissue and indicated a poor prognosis in patents. Overexpression of PIK3C3 in vitro repressed cell proliferation of KYSE-150 and TE-12 cells. Moreover, PIK3C3 overexpression was demonstrated to enhance the sensitivity of KYSE-150 and TE-12 cells to irradiation. In addition, miR-340-5p was revealed to directly bind and negatively modulate PIK3C3 expression in ESCC. Blockage of miR-340-5p promoted ESCC cell proliferation, while rescue of PIK3C3 reversed this effect. MiR-340-5p was highly expressed in ESCC tissue and it exhibited a negative correlation with PIK3C3 expression. Conclusions: MiR-340-5p functioned as an oncogene of ESCC by directly binding and repressing the expression of PIK3C3.

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MicroRNA-33a-5p suppresses esophageal squamous cell carcinoma progression via regulation of lncRNA DANCR and ZEB1

Cited by 27 publications

References 21 publications

<p>Long Noncoding RNA <em>FGD5-AS1</em> Acts as a Competing Endogenous RNA on microRNA-383 to Enhance the Malignant Characteristics of Esophageal Squamous Cell Carcinoma by Increasing SP1 Expression</p>

<p>Long Noncoding RNA <em>FGD5-AS1</em> Acts as a Competing Endogenous RNA on microRNA-383 to Enhance the Malignant Characteristics of Esophageal Squamous Cell Carcinoma by Increasing SP1 Expression</p>

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

PIK3C3 Acts as a Tumor Suppressor in Esophageal Squamous Cell Carcinoma and Was Regulated by MiR-340-5p

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