Lnc-NEAT1 induces cell apoptosis and inflammation but inhibits proliferation in a cellular model of hepatic ischemia/reperfusion injury

Abstract

Objective We aimed to investigate the effect of long non-coding RNA nuclear-enriched abundant transcript 1 (lnc-NEAT1) on regulating hepatocyte proliferation, apoptosis, and inflammation during hepatic ischemia/reperfusion (I/R) injury. Methods Human liver cells (HL-7702) were cultured under glucose-free and oxygen-free conditions to construct the I/R injury model. Expression of lnc-NEAT1 was detected in this model and in normal cells. Plasmids of control overexpression [NC(+)], lnc-NEAT1 overexpression [NEAT1(+)], control short hairpin (sh)RNA [NC(−)], and lnc-NEAT1 shRNA [NEAT1(−)] were transfected into HL-7702 cells and subsequently subjected to I/R treatment. Cell proliferation, apoptosis, apoptosis-related proteins, and inflammatory cytokines were assessed. Results Lnc-NEAT1 expression was elevated in the I/R group compared with the normal group. Cell proliferation was decreased in the NEAT1(+) group compared with the NC(+) group but increased in NEAT1(−) compared with NC(−). The apoptosis rate increased in the NEAT1(+) group compared with the NC(+) group but decreased in NEAT1(−) compared with NC(−). Western blot assay (detection of apoptosis-related proteins) showed similar results. Expression of interleukin-1β, interleukin-6, and tumor necrosis factor-α increased in the NEAT1(+) group compared with NC(+) but decreased in NEAT1(−) compared with NC(−). Conclusion Lnc-NEAT1 is overexpressed, induces cell apoptosis and inflammation, and inhibits proliferation during hepatic I/R injury.

Evodiamine inhibits malignant progression of ovarian cancer cells by regulating lncRNA‐NEAT1/miR‐152‐3p/CDK19 axis

“…NEAT1 has been demonstrated in several studies as a tumor‐promoting factor in ovarian cancer via targeting miRNAs (Chai et al, 2016; Yong et al, 2018). NEAT1 also promotes cell proliferation and induces apoptosis in liver cancer (Kou et al, 2020) and a cellular model of hepatic ischemia/reperfusion injury (Wang et al, 2021), while inhibiting apoptosis of neuron (Chai et al, 2022) and tubular epithelial cells (Ma et al, 2022). Herein, we identified that the NEAT1‐miR‐152‐3p axis is one of the mechanisms by which EVO alters the malignant biological behaviors of ovarian cancer cells.…”

Aberrant expressions of circulating lncRNA NEAT1 and microRNA‐125a are linked with Th2 cells and symptom severity in pediatric allergic rhinitis

“…(2) The lnc-NEAT1 expression was positively related to several inflammatory cytokines (including IL-1β and IL-6), which were reported to be increased in the AR patients than in controls. 14,18,26,27 Therefore, lnc-NEAT1 was overexpressed in pediatric AR patients than in DCs and HCs. (3) In terms of miR-125a, it could also regulate the homeostasis of Th1 and Th2 cells as well as suppress inflammation via stabilizing signal transducer and activator of transcription 3 (STAT3) activity and inhibiting immune responses.…”

lncRNA DHFRL1‑4 knockdown attenuates cerebral ischemia/reperfusion injury by upregulating the levels of angiogenesis‑related genes

“…A number of lncRNAs have been found to be associated with the severity and prognosis of ischemic stroke, and inflammation (18)(19)(20). For example, the levels of lncNEAT1 have been found to be elevated in cells following ischemia/reperfusion (I/R), inducing cell apoptosis and inflammation; the knockdown of lncNEAT1 has been found to reduce I/R-induced apoptosis (21). In addition, a recent study demonstrated that FOXD3 antisense RNA 1 (FOXD3-AS1) was upregulated in response to ischemic injury in cardiomyocytes (22).…”