Overexpression of long non-coding RNA SBF2-AS1 promotes cell progression in esophageal squamous cell carcinoma (ESCC) by repressing miR-494 to up-regulate PFN2 expression

Zhang, Qiu; Pan, X X; You, D Y

doi:10.1242/bio.048793

Cited by 13 publications

(11 citation statements)

References 4 publications

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“…Moreover, miR-494, in the present study was found to be underexpressed while TGIF1 was overexpressed in ESCC tissues and cells. In accordance to this finding, downregulation of miR-494 has been identified in EC by multiple functional reports [ 15 , 40 , 41 ]. However, overexpression of miR-494 harbors the potential to curb the proliferative and invasive capabilities of EC cells and to trigger apoptosis by targeting CLPTM1L [ 15 ].…”

Section: Discussionsupporting

confidence: 77%

Silencing of histone deacetylase 3 suppresses the development of esophageal squamous cell carcinoma through regulation of miR-494-mediated TGIF1

et al. 2022

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Background Deacetylation of histones by histone deacetylase 3 (HDAC3) acts importantly in modulating apoptosis, DNA damage and cellular progression. Herein, we aimed to unravel the functional role of HDAC3 in a lethal disease, esophageal squamous cell carcinoma (ESCC). Methods The expression of HDAC3 in clinically collected ESCC tissues was determined by RT-qPCR and immunohistochemistry. As revealed from bioinformatics analysis, the putative relations between HDAC3 and microRNA-494 (miR-494) and between miR-494 and transforming growth factor beta (TGFβ)-inducing factor 1 (TGIF1) were further verified by chromatin immunoprecipitation and dual-luciferase reporter gene assay. Functional roles of shRNA-mediated depletion of HDAC3, miR-494 mimic and overexpressed TGIF1 were explored by gain- and loss-of-function assays with regard to ESCC cell biological behaviors. A nude mouse model of ESCC was developed for in vivo validation. Results HDAC3 was highly expressed in ESCC tissues, suggestive of poor prognosis while TGIF1 was upregulated and miR-494 was downregulated. Mechanistic investigation revealed that HDAC3 inhibited miR-494 expression and TGIF1 was a direct target of miR-494. Furthermore, silencing HDAC3 or overexpressing miR-494 was demonstrated to suppress aggressive phenotypes of ESCC cells both in vitro through the activated TGFβ signaling pathway and in vivo, while TGIF1 overexpression induced opposite results. Conclusion Collectively, our findings provided demonstration regarding the oncogenic property of HDAC3 in ESCC via the miR-494/TGIF1/TGFβ axis.

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Section: Discussionsupporting

confidence: 77%

Silencing of histone deacetylase 3 suppresses the development of esophageal squamous cell carcinoma through regulation of miR-494-mediated TGIF1

et al. 2022

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“…Pioneering studies demonstrated that alterations of these genes might result in tumorigenesis and development; these include SMAD5 (24,25), IL7R (26), MAP2K6 (27), and PFN2 (28,29).…”

Section: Discussionmentioning

confidence: 99%

“…In the top 20 KEGG pathways, we identified cancer-related pathways, including the TGF-β signaling pathway (involving SMAD5), the PI3K-Akt signaling pathway (involving IL7R), the Jak-STAT signaling pathway (involving IL7R), the MAPK signaling pathway (involving genes MAP2K6), the Rap1 signaling pathway (involving MAP2K6 and PFN2), and cell adhesion molecules (involving PTPRC) ( Table 2 ). Pioneering studies demonstrated that alterations of these genes might result in tumorigenesis and development; these include SMAD5 ( 24 , 25 ), IL7R ( 26 ), MAP2K6 ( 27 ), and PFN2 ( 28 , 29 ).…”

Section: Discussionmentioning

confidence: 99%

Transcriptome Analysis of Ivosidenib-Mediated Inhibitory Functions on Non-Small Cell Lung Cancer

Chen

Shen

et al. 2021

Front. Oncol.

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Ivosidenib is an isocitrate dehydrogenase mutant inhibitor that the US Food and Drug Administration recently approved for the treatment of leukemia. Studies suggested that ivosidenib may inhibit the progression of non-small cell lung cancer (NSCLC). In the present study, we explored RNAs and their potential regulatory mechanisms by which ivosidenib treats NSCLC cells. We used MTT assays, Transwell assays, and flow cytometry to measure the anti-tumor effects of ivosidenib in NSCLC cells. We performed whole transcriptome sequencing to determine differentially expressed mRNAs (DE-mRNAs) and non-coding RNAs (ncRNA). We used GO and KEGG pathway enrichment analyses to identify the functions and potential mechanisms. According to miRNA target interactions, we constructed a competing endogenous network. Ivosidenib inhibited the proliferation, invasion, and migration of NSCLC cells and inhibited tumor growth in vivo. We identified 212 DE-mRNAs, four DE-miRNAs, and 206 DE-lncRNAs in ivosidenib-treated NSCLC cells compared to untreated NSCLC cells. DE-mRNAs were significantly enriched in the cancer-associated pathways, including the TGF-β signaling pathway, the PI3K-Akt signaling pathway, the Jak-STAT signaling pathway, the MAPK signaling pathway, the Rap1 signaling pathway, and cell adhesion molecules. Based on the competing endogenous RNA hypothesis, we constructed lncRNA-miRNA-mRNA networks to elucidate the regulatory relationships between mRNA and ncRNA. We found that qRT-PCR results showed corresponding expression trends of differential genes with sequencing data. Our results provide insights into the molecular basis of ivosidenib suppression of NSCLC.

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“… 21 MiR‐494‐3p has been confirmed to repress ESCC malignancy by targeting CLPTM1L 22 and PFN2. 23 Nevertheless, the function of miR‐494‐3p in the resistance of ESCC to DDP remains unclear.…”

Section: Introductionmentioning

confidence: 99%

“…Liu et al manifested that downregulation of miR‐455‐3p repressed chemoresistance and tumorigenesis in ESCC 21 . MiR‐494‐3p has been confirmed to repress ESCC malignancy by targeting CLPTM1L 22 and PFN2 23 . Nevertheless, the function of miR‐494‐3p in the resistance of ESCC to DDP remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Hsa_circ_0007142 contributes to cisplatin resistance in esophageal squamous cell carcinoma via miR‐494‐3p/LASP1 axis

Chang

Zhao

et al. 2022

Clinical Laboratory Analysis

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Background Chemoresistance is one of the major obstacles for tumor treatment. Circular RNAs (circRNAs) have been confirmed to play vital roles in chemoresistance of cancer, including esophageal squamous cell carcinoma (ESCC). We investigated the roles and mechanisms of circ_0007142 in cisplatin (DDP) resistance of ESCC. Methods Quantitative real‐time polymerase chain reaction (qRT‐PCR) was conducted to determine the levels of circ_0007142, DOCK1 mRNA, microRNA‐494‐3p (miR‐494‐3p) and LIM And SH3 Protein 1 (LASP1) mRNA. RNase R assay was conducted to analyze the characteristic of circ_0007142. Cell Counting Kit‐8 (CCK‐8) assay was performed to evaluate IC50 of DDP. Flow cytometry analysis, 5‐ethynyl‐2’‐deoxyuridine (EdU) assay and transwell assay were carried out to examine cell apoptosis, proliferation and invasion, respectively. Dual‐luciferase reporter assay was employed to verify the association between miR‐494‐3p and circ_0007142 or LASP1. Murine xenograft assay was conducted to investigate the role of circ_0007142 in DDP resistant in vivo. The protein level of LASP1 in tumors was measured by Immunohistochemistry (IHC) analysis. Results Circ_0007142 was upregulated in DDP‐resistant ESCC tissues and cells. Circ_0007142 knockdown improved DDP sensitivity, induced cell apoptosis and hampered cell proliferation and invasion in DDP‐resistant ESCC cells. Circ_0007142 functioned as the sponge for miR‐494‐3p and miR‐494‐3p inhibition reversed the impacts of circ_0007142 knockdown on DDP resistance, cell apoptosis, proliferation, and invasion. LASP1 was a target of miR‐494‐3p, and the effects on DDP resistance, cell apoptosis, growth, and invasion mediated by LASP1 downregulation were rescued by miR‐494‐3p inhibition. Moreover, circ_0007142 knockdown enhanced DDP sensitivity in vivo. Conclusion Circ_0007142 improved DDP resistance of ESCC by upregulating LASP1 via sponging miR‐494‐3p.

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Overexpression of long non-coding RNA SBF2-AS1 promotes cell progression in esophageal squamous cell carcinoma (ESCC) by repressing miR-494 to up-regulate PFN2 expression

Cited by 13 publications

References 4 publications

Silencing of histone deacetylase 3 suppresses the development of esophageal squamous cell carcinoma through regulation of miR-494-mediated TGIF1

Silencing of histone deacetylase 3 suppresses the development of esophageal squamous cell carcinoma through regulation of miR-494-mediated TGIF1

Transcriptome Analysis of Ivosidenib-Mediated Inhibitory Functions on Non-Small Cell Lung Cancer

Hsa_circ_0007142 contributes to cisplatin resistance in esophageal squamous cell carcinoma via miR‐494‐3p/LASP1 axis

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