&lt;p&gt;Long Noncoding RNA GAS5 Acts As A Tumor Suppressor In Laryngeal Squamous Cell Carcinoma Via miR-21 [Corrigendum]&lt;/p&gt;

Lyu, Kexing; Xu, Yang; Yue, Huijun; Li, Yun; Zhao, Jing; Chen, Lin; Wu, Jianhui; Zhu, Xiaolin; Chai, Liping; Li, Chunwei; Wen, Wang; Lei, Wenbin

doi:10.2147/cmar.s232421

Cited by 4 publications

(7 citation statements)

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“…More and more studies have proved that lncRNAs play a crucial role in the multi‐steps of tumour development 17 . For instance, lncRNA growth arrest‐specific 5 (GAS5) suppresses LSCC progression through the negative regulation of miR‐21 and its targets involved in cell proliferation and apoptosis 18 . Our previous research has demonstrated that lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) regulates CDK6 expression mediated by miR‐107 in LSCC, which may be a potential target for therapeutic intervention of LSCC 19 .…”

Section: Introductionmentioning

confidence: 99%

“…17 For instance, lncRNA growth arrest-specific 5 (GAS5) suppresses LSCC progression through the negative regulation of miR-21 and its targets involved in cell proliferation and apoptosis. 18 Our previous research has demonstrated that lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) regulates CDK6 expression mediated by miR-107 in LSCC, which may be a potential target for therapeutic intervention of LSCC. 19 It has been proved that m6A-methylated level can affect the expression of lncRNA, and regulate the development of tumour.…”

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confidence: 99%

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ALKBH5‐mediated m6A modification of lncRNA KCNQ1OT1 triggers the development of LSCC via upregulation of HOXA9

Yan

Wang

et al. 2021

J Cellular Molecular Medi

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Laryngeal squamous cell carcinoma (LSCC) is the most common pathological subtype (>95%) of laryngeal carcinoma. 1,2 The prevalence of LSCC was ranked as 2nd in head and neck squamous cell carcinoma (HNSCC). It is reported that in 2018, there were 177,422 new cases of LSCC and 94,771 deaths of LSCC in the world. 3 Notably, the incidence of LSCC in China is about four times that in the United States, with an estimated death toll of more than 15,000 per year. 4 The 5-year overall survival (OS) rate of patients with advanced LSCC is lower than 50%. 5 Therefore, we urgently need to have a deeper understanding of the mechanism that promotes LSCC progression. N6-methyladenosine (m6A) as a major internal modification of RNA in higher eukaryotes has aroused great interest in recent years. [6][7][8] The researchers suggested that the m6A methylation plays an important role in the regulation of gene expression by influencing RNA stability, mRNA degradation and translation. 9,10 This modification mainly depends on the dynamic regulation of RNA

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Section: Introductionmentioning

confidence: 99%

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confidence: 99%

ALKBH5‐mediated m6A modification of lncRNA KCNQ1OT1 triggers the development of LSCC via upregulation of HOXA9

Yan

Wang

et al. 2021

J Cellular Molecular Medi

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“…13 Furthermore, Lyu et al showed that lncRNA GAS5 inhibited cell proliferation and increased the cell apoptosis rate in laryngeal squamous cell carcinoma by regulating the miR-21/BAX/CDK6 axis. 14 However, Lyu’s study had some limitations. 14 First, the function and relative regulatory mechanism of lncRNA GAS5 on laryngeal cancer cell migration and invasion ability in vitro have not been elucidated.…”

Section: Introductionmentioning

confidence: 99%

“…14 However, Lyu’s study had some limitations. 14 First, the function and relative regulatory mechanism of lncRNA GAS5 on laryngeal cancer cell migration and invasion ability in vitro have not been elucidated. Second, in vivo animal experiments have not yet been performed.…”

Section: Introductionmentioning

confidence: 99%

Upregulation of Long Noncoding RNA_GAS5 Suppresses Cell Proliferation and Metastasis in Laryngeal Cancer via Regulating PI3K/AKT/mTOR Signaling Pathway

Liu

Zhan

Zhong

et al. 2021

Technol Cancer Res Treat

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Background: Laryngeal cancer is one of the most common malignant tumors among head and neck cancers. Accumulating studies have indicated that long noncoding RNAs (lncRNAs) play an important role in laryngeal cancer occurrence and progression, however, the functional roles and relative regulatory mechanisms of lncRNA growth arrest-specific transcript 5 (GAS5) in laryngeal cancer progression remain unclear. Methods: The expression of lncRNA GAS5 in both laryngeal cancer tissues and cell lines was evaluated using quantitative reverse transcription-polymerase chain reaction (RT-qPCR) assay. The relationships between lncRNA GAS5 expression and clinical parameters were also analyzed. To determine the biological function of lncRNA GAS5, a lncRNA GAS5-specific plasmid was first transfected into laryngeal cancer cells using lentiviral technology. Cell counting kit-8 assay, flow cytometry, and Transwell assays were used to detect in vitro cell proliferation, apoptosis, cycle distribution, and metastasis abilities, respectively. Furthermore, in vivo cell growth experiments were also performed using nude mice. Additionally, western blotting was performed to identify the underlying regulatory mechanism. Results: In the current study, lncRNA GAS5 was downregulated in laryngeal cancer tissues and its low expression was closely associated with poor tumor differentiation, advanced TNM stage, lymph node metastasis, and shorter overall survival time. In addition, lncRNA GAS5 upregulation significantly inhibited laryngeal cancer cell proliferation both in vitro and in vivo. Moreover, in response to lncRNA GAS5 overexpression, more laryngeal cancer cells were arrested at the G2/M stage, accompanied by increased cell apoptosis rates and suppressed migration and invasion capacities. Mechanistically, our data showed that the overexpression of lncRNA GAS5 significantly regulated the PI3K/AKT/mTOR signaling pathway. Conclusion: LncRNA GAS5 might act as a suppressor gene during laryngeal cancer development, as it suppressed cell proliferation and metastasis by regulating the PI3K/AKT/mTOR signaling pathway; thus, lncRNA GAS5 is a promising therapeutic biomarker for the treatment of laryngeal cancer.

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“…Furthermore, long intergenic non-protein coding RNA 987 mitigates COPD by regulating lipopolysaccharide (LPS)-caused cell apoptosis, oxidative stress, inflammation and autophagy via the Let-7b-5p/sirtuin1 axis ( 30 ). Growth arrest-specific 5 (GAS5), a well-documented lncRNA, is an important factor associated with cell proliferation and death in various diseases ( 31 , 32 ). GAS5 acts as a ceRNA to sponge miR-223-3p in certain diseases.…”

Section: Introductionmentioning

confidence: 99%

lncRNA GAS5 promotes pyroptosis in COPD by functioning as a ceRNA to regulate the miR‑223‑3p/NLRP3 axis

Chen

et al. 2022

Mol Med Rep

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Chronic obstructive pulmonary disease (COPD) is characterized by irreversible and progressive airflow limitation and encompasses a spectrum of diseases, including chronic obstructive bronchitis and emphysema. Pyroptosis is a unique form of inflammatory cell death mediated by the activation of caspase-1 and inflammasomes. The long non-coding RNA (lncRNA) growth arrest-specific 5 (GAS5) is a well-documented tumor suppressor, which is associated with cell proliferation and death in various diseases. The aim of the present study was to evaluate whether lncRNA GAS5 is associated with the pyroptosis in COPD. To create a COPD cell model, MRC-5 cells were treated with 10 µg/ml lipopolysaccharide (LPS) for 48 h. Then the level of pro-caspase 1, caspase 1, IL-1β, IL-18, NLRP3 and cleaved gasdermin D (GSDMD) was examined by western blotting. GAS5 mRNA level was detected by qualitative PCR following LPS treatment in MRC-5 cells. Subsequently, IL-2, IL-6, IL-10 and TNF-α in MRC-5 cells was measured by ELISA. Then the proliferation ability of MRC-5 cells was detected by CCK-8. Cell death was detected by TUNEL assay. LDH release was measured using an LDH Cytotoxicity Assay kit. The Magna RIP kit was used to validate the interaction between GAS5 and miR-223-3p. The present study revealed that increased expression levels of caspase-1, IL-1β, IL-18 and cleaved GSDMD were observed in LPS-treated MRC-5 cells, indicating that pyroptosis is involved in COPD progression. Additionally, LPS induced the increase in GAS5 mRNA expression levels and the release of inflammatory factors (IL-2, IL-6, IL-10 and TNF-α), suggesting that GAS5 is implicated in pyroptosis in COPD. Furthermore, upregulation of GAS5 promoted cell death and inhibited proliferation in the MRC-5 cell line. Additionally, increased GAS5 expression significantly promoted the production of caspase-1, IL-1β, IL-18, cleaved GSDMD and NLR pyrin domain containing protein 3 (NLRP3). A dual-luciferase assay demonstrated that GAS5 could directly bind to microRNA-223-3p (miR-223-3p), and NLRP3 is a direct target of miR-223-3p. Furthermore, GAS5 reduced the expression levels of miR-223-3p, while it increased the expression levels of NLRP3. The present study concluded that lncRNA GAS5 promoted pyroptosis in COPD by targeting the miR-223-3p/NLRP3 axis, implying that GAS5 could be a potential target for COPD.

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<p>Long Noncoding RNA GAS5 Acts As A Tumor Suppressor In Laryngeal Squamous Cell Carcinoma Via miR-21 [Corrigendum]</p>

Cited by 4 publications

References 0 publications

ALKBH5‐mediated m6A modification of lncRNA KCNQ1OT1 triggers the development of LSCC via upregulation of HOXA9

ALKBH5‐mediated m6A modification of lncRNA KCNQ1OT1 triggers the development of LSCC via upregulation of HOXA9

Upregulation of Long Noncoding RNA_GAS5 Suppresses Cell Proliferation and Metastasis in Laryngeal Cancer via Regulating PI3K/AKT/mTOR Signaling Pathway

lncRNA GAS5 promotes pyroptosis in COPD by functioning as a ceRNA to regulate the miR‑223‑3p/NLRP3 axis

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