Long non-coding antisense RNA GAS6-AS1 supports gastric cancer progression via increasing GAS6 expression

Zhang, Peichen; Dong, Qian-Tong; Zhu, Hua; Shi, Li; Shi, Lingyan; Chen, Xiangjian

doi:10.1016/j.gene.2018.12.079

Cited by 37 publications

(38 citation statements)

References 38 publications

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“…Previous research revealed that low expression of GAS6-AS1 predicted a poor prognosis in patients with NSCLC [40]. And GAS6-AS1 was identi ed to play vital roles in the progression of gastric cancer and hepatocellular carcinoma [41,42]. In our study, we further found that the expression of GAS6-AS1 was frequently downregulated in LUAD tissues and clinical analysis reveals that downregulation of GAS6-AS1 correlated with advanced tumor stage and poor prognosis of LUAD patients.…”

Section: Discussionsupporting

confidence: 65%

Long Noncoding RNA GAS6-AS1 Inhibits Progression and Glucose Metabolism Reprogramming in Lung Adenocarcinoma Via Repressing E2F1-Mediated Transcription of GLUT1

Wang

et al. 2020

Preprint

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BackgroundGlucose metabolism reprogramming is one of the hallmarks of cancer cells. While functional and regulatory mechanism of long noncoding RNA (lncRNA) in the contribution of glucose metabolism in lung adenocarcinoma (LUAD) remains incompletely understood. The aim of this study was to uncover the roles for GAS6-AS1 in the regulation of progression and glucose metabolism in LUAD.MethodsThe tumor-suppressive function of GAS6-AS1 was determined by experiments in vitro and nude mice xenograft models. The role of GAS6-AS1 in regulating cancer glucose metabolism was proved by detecting glucose uptake, lactate production, pyruvate production and extracellular acidification rate (ECAR). RNA pull-down assay, RNA immunoprecipitation (RIP) assay, luciferase reporter assay and Chromatin Immunoprecipitation (ChIP) assay were used to identify the underlying molecular mechanisms of GAS6-AS1. And the expression level of GAS6-AS1 in LUAD tissues and cells was measured by quantitative real-time PCR.ResultsOverexpression of GAS6-AS1 suppressed tumor progression of LUAD both in vitro and in vivo. Metabolic-related assays revealed that GAS6-AS1 inhibited glucose metabolism reprogramming. Mechanically, GAS6-AS1 was found to repress the expression of glucose transporter GLUT1, a key regulator of glucose metabolism. Ectopic expression of GLUT1 restored the inhibition effect of GAS6-AS1 on cancer progression and glucose metabolism reprogramming. Further investigation identified that GAS6-AS1 directly interacted with transcription factor E2F1 and suppressed E2F1-mediated transcription of GLUT1. And GAS6-AS1 was downregulated in LUAD tissues and correlated with clinicopathological characteristics and survival of patients.ConclusionsTaken together, our results identified GAS6-AS1 as a novel tumor suppressor in LUAD and unraveled its underlying molecular mechanism in reprogramming glucose metabolism. GAS6-AS1 potentially served as a prognostic marker and therapeutic target in LUAD.

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Section: Discussionsupporting

confidence: 65%

Long Noncoding RNA GAS6-AS1 Inhibits Progression and Glucose Metabolism Reprogramming in Lung Adenocarcinoma Via Repressing E2F1-Mediated Transcription of GLUT1

Wang

et al. 2020

Preprint

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“…LncRNAs are a new class of ncRNAs longer than 200 nt and have no protein coding potential. Based on the positions and characteristics in human genome, lncRNAs can be divided into five categories: sense, antisense, bidirectional, intronic and intergenic lncRNAs [117][118][119][120]. Multiple lncRNAs are aberrantly expressed in HCC and are significantly associated with metastasis, recurrence, prognosis and chemoresistance through various mechanisms, including interactions with DNA, RNA or proteins to form complexes that regulate the expression of target genes [118,[121][122][123][124][125][126][127][128][129][130].…”

Section: Lncrnas and Therapy Resistancementioning

confidence: 99%

The emerging role of microRNAs and long noncoding RNAs in drug resistance of hepatocellular carcinoma

et al. 2019

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Hepatocellular carcinoma (HCC) is the fifth most common malignancy worldwide and the second most lethal human cancer. A portion of patients with advanced HCC can significantly benefit from treatments with sorafenib, adriamycin, 5-fluorouracil and platinum drugs. However, most HCC patients eventually develop drug resistance, resulting in a poor prognosis. The mechanisms involved in HCC drug resistance are complex and inconclusive. Human transcripts without protein-coding potential are known as noncoding RNAs (ncRNAs), including microRNAs (miRNAs), small nucleolar RNAs (snoRNAs), long noncoding RNAs (lncRNAs) and circular RNA (circRNA). Accumulated evidences demonstrate that several deregulated miRNAs and lncRNAs are important regulators in the development of HCC drug resistance which elucidates their potential clinical implications. In this review, we summarized the detailed mechanisms by which miRNAs and lncRNAs affect HCC drug resistance. Multiple tumorspecific miRNAs and lncRNAs may serve as novel therapeutic targets and prognostic biomarkers for HCC.

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“…GAS6 is a ligand for AXL receptor tyrosine kinase, which further activates downstream pro‐survival signals . Therefore, GAS6 has been revealed to have oncogenic roles in many cancers . To assess whether GAS6‐AS2 also regulates GAS6 in melanoma, we first detected GAS6 mRNA expression levels in GAS6‐AS2 stably overexpressed and depleted melanoma cells.…”

Section: Resultsmentioning

confidence: 99%

“…33,34 Therefore, GAS6 has been revealed to have oncogenic roles in many cancers. [35][36][37] To assess whether GAS6-AS2 also regulates GAS6 in melanoma, we first detected GAS6 mRNA expression levels in GAS6-AS2 stably overexpressed and depleted melanoma cells. As shown in Figure 5a,b, ectopic expression of GAS6-AS2 increased GAS6 mRNA levels, and while knockdown of GAS6-AS2 decreased GAS6 mRNA levels.…”

Section: Gas6-as2 Upregulates Gas6 Expression and Activates Axl/aktmentioning

confidence: 99%

Increased expression of long noncoding RNA GAS6‐AS2 promotes proliferation and inhibits apoptosis of melanoma cells via upregulating GAS6 expression

et al. 2019

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Long noncoding RNAs (lncRNAs) are frequently aberrantly expressed and involved in many cancers, including melanoma. GAS6‐AS2 was a recently identified cancer‐related lncRNA. However, the expression, roles, and functional mechanisms of GAS6‐AS2 in melanoma remain unknown. In this study, we found that lncRNA GAS6‐AS2 is significantly elevated in melanoma tissues and cells. Elevated expression of GAS6‐AS2 is positively correlated with advanced stages and poor prognosis in melanoma. Functional assays demonstrated that ectopic expression of GAS6‐AS2 promotes proliferation and inhibits apoptosis of melanoma cells. In contrast, knockdown of GAS6‐AS2 inhibits proliferation and promotes apoptosis of melanoma cells. Furthermore, in vivo functional assays showed that GAS6‐AS2 promotes melanoma xenograft growth. Mechanistically, we found that GAS6‐AS2 upregulates GAS6 expression, promotes GAS6 secretion, and activates AXL/AKT/ERK signals. The expression of GAS6 was positively correlated with that of GAS6‐AS2 in melanoma tissues. In addition, deficiency of GAS6 reverses the biological roles of GAS6‐AS2 overexpression in melanoma cell proliferation and apoptosis. Collectively, our data identified GAS6‐AS2 as an oncogenic lncRNA in melanoma via activation of GAS6/AXL/AKT/ERK signals. Our data suggested that GAS6‐AS2 may be a novel potential prognostic biomarker and therapeutic target for melanoma.

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Long non-coding antisense RNA GAS6-AS1 supports gastric cancer progression via increasing GAS6 expression

Cited by 37 publications

References 38 publications

Long Noncoding RNA GAS6-AS1 Inhibits Progression and Glucose Metabolism Reprogramming in Lung Adenocarcinoma Via Repressing E2F1-Mediated Transcription of GLUT1

Long Noncoding RNA GAS6-AS1 Inhibits Progression and Glucose Metabolism Reprogramming in Lung Adenocarcinoma Via Repressing E2F1-Mediated Transcription of GLUT1

The emerging role of microRNAs and long noncoding RNAs in drug resistance of hepatocellular carcinoma

Increased expression of long noncoding RNA GAS6‐AS2 promotes proliferation and inhibits apoptosis of melanoma cells via upregulating GAS6 expression

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