LncRNA CASC2 is involved in the development of chronic obstructive pulmonary disease <i>via</i> targeting miR-18a-5p/IGF1 axis

Li, Panpan; Zhang, Huali; Zeng, Haizhu; Meng, Yingxia; Gao, Hongchang; Zhang, Meilan; Zhao, Lei

doi:10.1177/17534666211028072

Cited by 14 publications

(13 citation statements)

References 35 publications

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“…Furthermore, ceRNA networks have also been reported to regulate the progression of COPD. lncRNA SNHG5, cancer susceptibility 2 and RP11-86H7.1 have all been reported to serve as miRNA sponges and keep miRNA away from its target genes through ceRNA networks to serve important roles in the progression of COPD ( 28 , 68 , 69 ). However, to the best of our knowledge, at present, no study has reported the role of GAS5 in COPD.…”

Section: Discussionmentioning

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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Section: Discussionmentioning

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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“… 10 The above evidence reveals that lncRNA CASC2 hinders organ injuries through various pathways. 10 , 11 , 12 , 17 , 19 Thus, this study further assessed the relationship between lncRNA CASC2 and multi‐organ injuries in sepsis patients. It was clear that lncRNA CASC2 was inversely linked with multiple organ injuries (reflected by total SOFA score), as well as respiratory, coagulation, liver, and renal injury (reflected by SOFA sub‐scales) in sepsis patients.…”

Section: Discussionmentioning

confidence: 99%

Potential of circulating lncRNA CASC2 as a biomarker in reflecting the inflammatory cytokines, multi‐organ dysfunction, disease severity, and mortality in sepsis patients

Wang

Zhao

Wei

et al. 2022

Clinical Laboratory Analysis

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Background: Long noncoding RNA (lncRNA) cancer susceptibility candidate gene 2 (CASC2) inhibits inflammation and multi-organ dysfunction in various ways. The present study was intended to explore the potency of blood lncRNA CASC2 as a biomarker for sepsis management.Methods: Totally, 184 sepsis patients and 30 healthy controls were enrolled. The reverse transcription-quantitative polymerase chain reaction was used to detect lncRNA CASC2 expression in peripheral blood mononuclear cell samples from the subjects. Mortality during 28 days was recorded in sepsis patients. Results: LncRNA CASC2 was decreased in sepsis patients [median (interquartile range [IQR]): 0.473 (0.241-0.773)] by comparison to healthy controls [median (IQR): 1.019 (0.676-1.685)] (p < 0.001). In sepsis patients, lncRNA CASC2 was negatively correlated with Acute Physiology and Chronic Health Evaluation II (APACHE II) (p = 0.001),Sequential Organ Failure Assessment (SOFA) (p < 0.001), SOFA-respiratory system (p = 0.010), SOFA-coagulation (p = 0.020), SOFA-liver (p = 0.019), and SOFA-renal (p = 0.010) scores, but was not related to SOFA-nervous (p = 0.466) and SOFA-cardio vascular system (p = 0.059) scores. Additionally, lncRNA CASC2 was negatively related to tumor necrosis factorα (p = 0.024), interleukin (IL)-1β (p = 0.013), and IL-17A (p = 0.002), but was not linked to IL-6 (p = 0.112) or IL-10 (p = 0.074). Furthermore, lncRNA CASC2 was lower in sepsis deaths [median (IQR): 0.286 (0.166-0.475)] than in survivors [median (IQR): 0.534 (0.296-0.811)] (p < 0.001). Simultaneously, Kaplan-Meier (KM) curve analysis also observed that lncRNA CASC2 was inversely related to accumulating mortality in sepsis patients (p = 0.003). While lncRNA CASC2 could independently predict lower mortality risk. Conclusion:Circulating lncRNA CASC2 inadequacy indicates the release of inflammatory cytokines, severe multi-organ injuries, and increased mortality in sepsis patients.

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“…CSE was prepared according to the previously reported method [ 16 ]. In short, a cigarette burns with a modified apparatus with a driving device.…”

Section: Methodsmentioning

confidence: 99%

Long non-coding RNA OIP5-AS1 regulates smoke-related chronic obstructive pulmonary disease via targeting micro RNA -410-3p/IL-13

et al. 2021

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This investigation aimed to assess the levels of serum OIP5-AS1 and micro RNA-410-3p (miR-410-3p) in patients with chronic obstructive pulmonary disease (COPD) and their potential molecular mechanism. The levels of OIP5-AS1 and miR-410-3p as well as mRNA levels of IL-13 were measured. Pearson variable linear test was applied to analyze the correlations between forced expiratory volume in 1 second (FEV1) and OIP5-AS1. The receiver operating characteristic curve was used to predict the predictive possibility of OIP5-AS1. The viable cells were detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and flow cytometry was used to detect the cell apoptosis. An enzyme-linked immunosorbent assay was performed to indicate the inflammatory situation of 16HBE cells. Luciferase activity assay was conducted to examine the relationships between OIP5-AS1 and miR-410-3p together with miR-410-3p and IL-13. Augmented levels of OIP5-AS1, declined levels of miR-410-3p, and enhanced expression of IL-13 were unveiled. The expression of OIP5-AS1 and miR-410-3p was related to the ratio of FEV1 respectively. OIP5-AS1 might serve as a diagnostic biomarker. Interference of OIP5-AS1 restored the abnormal cell viability, apoptosis, and inflammation in cigarette smoke extract (CSE)-stimulated 16HBE cells by regulating miR-410-3p and IL-13. OIP5-AS1 appeared to be a biomarker for distinguishing COPD patients from smokers. OIP5-AS1/miR-410-3p/IL-13 exerted function on the cell viability, apoptosis, and inflammation in CSE-steered cell models.

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LncRNA CASC2 is involved in the development of chronic obstructive pulmonary disease via targeting miR-18a-5p/IGF1 axis

Cited by 14 publications

References 35 publications

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

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

Potential of circulating lncRNA CASC2 as a biomarker in reflecting the inflammatory cytokines, multi‐organ dysfunction, disease severity, and mortality in sepsis patients

Long non-coding RNA OIP5-AS1 regulates smoke-related chronic obstructive pulmonary disease via targeting micro RNA -410-3p/IL-13

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