LncRNA FAM83A-AS1 promotes ESCC progression by regulating miR-214/CDC25B axis

Jia, Jinlin; Li, Hongle; Chu, Jie; Sheng, Jinxiu; Wang, Chang; Jia, Zimo; Meng, Weiwei; Yin, Hang; Wan, Junhu; He, Fucheng

doi:10.7150/jca.54007

Cited by 36 publications

(26 citation statements)

References 35 publications

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“…Many studies have reported that lncRNA, FAM83A-AS1 has potent tumor-promoting activity in oesophageal squamous cell carcinoma (ESCC), lung cancer, and liver carcinoma [25][26][27]. For instance, Xiao G et al [28] discovered that FAM83A-AS1 could promote LUAD cell migration and invasion, consistent with our results.…”

Section: Discussionsupporting

confidence: 91%

LncRNA FAM83A-AS1 facilitates tumor proliferation and the migration via the HIF-1α/ glycolysis axis in lung adenocarcinoma

Chen¹,

Hu²,

Sui³

et al. 2022

Int. J. Biol. Sci.

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Background: Lung adenocarcinoma (LUAD), the major subtype of lung cancer, is among the leading cause of cancer-related death worldwide. Energy-related metabolic reprogramming metabolism is a hallmark of cancer shared by numerous cancer types, including LUAD. Nevertheless, the functional pathways and molecular mechanism by which FAM83A-AS1 acts in metabolic reprogramming in lung adenocarcinoma have not been fully elucidated. Methods: We used transwell, wound-healing scratch assay, and metabolic assays to explore the effect of FAM83A-AS1 in LUAD cell lines. Western blotting, Co-IP assays, and ubiquitination assays were used to detect the effects of FAM83A-AS1 on HIF-1α expression, degradation, and its binding to VHL. Moreover, an in vivo subcutaneous tumor formation assay was used to detect the effect of FAM83A-AS1 on LUAD. Results: Herein, we identified FAM83A-AS1 as a metabolism-related lncRNA, which was highly correlated with glycolysis, hypoxia, and OXPHOS pathways in LUAD patients using bioinformatics analysis. In addition, we uncovered that FAM83A-AS1 could promote the migration and invasion of LUAD cells, as well as influence the stemness of LUAD cells in vivo and vitro. Moreover, FAM83A-AS1 was shown to promote glycolysis in LUAD cell lines in vitro and in vivo, and was found to influence the expression of genes related to glucose metabolism. Besides, we revealed that FAM83A-AS1 could affect glycolysis by regulating HIF-1α degradation. Finally, we found that FAM83A-AS1 knockdown could inhibit tumor growth and suppress the expression of HIF-1α and glycolysis-related genes in vivo. Conclusion:Our study demonstrates that FAM83A-AS1 contributes to LUAD proliferation and stemness via the HIF-1α/glycolysis axis, making it a potential biomarker and therapeutic target in LUAD patients.

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Section: Discussionsupporting

confidence: 91%

LncRNA FAM83A-AS1 facilitates tumor proliferation and the migration via the HIF-1α/ glycolysis axis in lung adenocarcinoma

Chen¹,

Hu²,

Sui³

et al. 2022

Int. J. Biol. Sci.

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“…In addition, FAM83A-AS1 may also strengthen the pre-mRNA stability of FAM83A to improve the metastatic ability of lung adenocarcinoma [ 54 ]. In esophageal cell squamous carcinoma, FAM83A-AS1 downregulation regulates the miR-214/CDC25B axis to suppress tumor cell growth, invasion and migration [ 55 ]. Furthermore, He and colleagues reported that FAM83A-AS1 was expressed in HCC cells and tissues, suggesting that increased FAM83A-AS1 expression enhances tumor proliferation and migration and represses apoptosis by interacting with NOP58 [ 56 ].…”

Section: Discussionmentioning

confidence: 99%

A novel pyroptosis-related lncRNA signature for prognostic prediction in patients with lung adenocarcinoma

et al. 2021

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Lung adenocarcinoma (LUAD) has been the major cause of tumor-associated mortality in recent years and has a poor prognosis. Pyroptosis is regulated via the activation of inflammasomes and participates in tumorigenesis. However, the effects of pyroptosis-related lncRNAs (PRlncRNAs) on LUAD have not yet been completely elucidated. Therefore, we attempted to systematically explore patterns of cell pyroptosis to establish a novel signature for predicting LUAD survival. Based on TCGA database, we set up a prognostic model by incorporating PRlncRNAs with differential expression using Cox regression and LASSO regression. Kaplan-Meier analysis was conducted to compare the survival of LUAD patients. We further simplified the risk model and created a nomogram to enhance the prediction of LUAD prognosis. Altogether, 84 PRlncRNAs with differential expression were discovered. Subsequently, a new risk model was constructed based on five PRlncRNAs, GSEC, FAM83A-AS1, AL606489.1, AL034397.3 and AC010980.2. The proposed signature exhibited good performance in prognostic prediction and was related to immunocyte infiltration. The nomogram exactly forecasted the overall survival of patients and had excellent clinical utility. In the present study, the five-lncRNA prognostic risk signature and nomogram are trustworthy and effective indicators for predicting the prognosis of LUAD.

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“…CircZNF609 promoted tumor growth through novel circZNF609/miR-1200/CDC25B axis, implying that circZNF609 has signi cant potential to serve as a new diagnostic biomarker and therapeutic target for BCa patients. lncRNA FAM83A-AS1 could promote esophageal cell squamous carcinoma progression by increasing CDC25B expression (Jia et al, 2021).According to our ndings, the circZNF609-mediated function network will provide new avenues for BCa treatment. Additonally, inhibitors of this network may serve as a potential adjuvant for cisplatin-based chemotherapy in BCa.…”

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confidence: 77%

mentioning

confidence: 99%

CircZNF609 Promotes Bladder Cancer Progression and Inhibits Cisplatin Sensitivity via miR-1200/CDC25B Pathway

Feng

et al. 2021

Preprint

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Circular RNAs (circRNAs) have been extensively studied in tumor development and treatment. CircZNF609 has been shown to act as an oncogene in a variety of solid tumors and may serve as a novel biomarker for tumor diagnosis and treatment. However, the underlying role and mechanism of circZNF609 in bladder cancer (BCa) development and cisplatin chemosensitivity were unknown. Quantitative real-time PCR (qRT-PCR) was applied to determine the expression of circZNF609, microRNA 1200 (miR-1200) and CDC25B in BCa cells and tissues. Western blot was used to detect the protein level of CDC25B. Functional assays in vitro and in vivo were conducted to investigate the effects of circZNF609 on tumor development and cisplatin chemosensitivity in BCa. RNA sequencing and online databases were used to predict the interactions among circZNF609, miR-1200 and CDC25B. Dual luciferase reporter assay, RNA pull-down assay and RNA fluorescence in situ hybridization (FISH) were applied to confirm the mechanism. CircZNF609 expression was significantly up-regulated in BCa cell lines and tissues. Increased expression of circZNF609 was related to a worse survival in BCa patients. In vitro and in vivo, enforced-expression of circZNF609 enhanced BCa cells proliferation, migration and cisplatin chemoresistance. Mechanistically, circZNF609 alleviated the inhibition effect on target CDC25B expression by sponging miR-1200. CircZNF609 promoted tumor growth through novel circZNF609/miR-1200/CDC25B axis, implying that circZNF609 has significant potential to serve as a new diagnostic biomarker and therapeutic target for BCa patients.

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LncRNA FAM83A-AS1 promotes ESCC progression by regulating miR-214/CDC25B axis

Cited by 36 publications

References 35 publications

LncRNA FAM83A-AS1 facilitates tumor proliferation and the migration via the HIF-1α/ glycolysis axis in lung adenocarcinoma

LncRNA FAM83A-AS1 facilitates tumor proliferation and the migration via the HIF-1α/ glycolysis axis in lung adenocarcinoma

A novel pyroptosis-related lncRNA signature for prognostic prediction in patients with lung adenocarcinoma

CircZNF609 Promotes Bladder Cancer Progression and Inhibits Cisplatin Sensitivity via miR-1200/CDC25B Pathway

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