Long non-coding RNA (LncRNA) SNHG7/ Eukaryotic translation initiation factor 4 gamma 2 (EIF4G2) involves in the malignant events of ovarian cancer cells with paclitaxel resistant

Zhang, Jin; Zhang, Rui; Ye, Yongju

doi:10.1080/21655979.2021.1999555

Cited by 7 publications

(6 citation statements)

References 28 publications

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“…Cell cycle research revealed that EIF4G2 silencing led to a rise in cells in the G0/G1 phase and a drop in cells in the G2/M phase (36). EIF4G2 promotes cell proliferation in a variety of tissues, such as chondrocytes and ovarian cancer (37)(38)(39). EIF4G2 has also been proven to have a strong proliferative effect on human colon cancer cells, and its expression is increased in skeletal muscle after I/R (36,40).…”

Section: Discussionmentioning

confidence: 99%

miR-379-5P INHIBITION ENHANCES INTESTINAL EPITHELIAL PROLIFERATION AND BARRIER FUNCTION RECOVERY AFTER ISCHEMIA/REPERFUSION BY TARGETING EIF4G2

Jia,

Wang,

Gao

et al. 2023

Shock

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Gut barrier dysfunction caused by intestinal ischemia/reperfusion (I/R) injury is associated with substantial death and morbidity. In this research, the role of microRNAs (miRNAs) in regulating intestinal I/R injury was investigated. We used miRNA sequencing to analyze clinical ischemic and normal intestinal samples. Through bioinformatics analysis based on sequencing results, we found that upregulated miRNAs inhibited epithelial barrier function and cell proliferation, with miR-379-5p being the most significantly upregulated in the ischemic intestine. Further studies confirmed the role of miR-379-5p through experiments in the human ischemic intestine, the mouse I/R injury model in vivo, and cell hypoxia/reoxygenation models in vitro. Inhibiting miR-379-5p increased epithelial cell proliferation and improved barrier function after I/R injury. We also identified eukaryotic translation initiation factor 4 gamma 2 (EIF4G2) as a downstream target gene of miR-379-5p through bioinformatics prediction and experimental verification. The findings suggest that inhibiting miR-379-5p could improve intestinal epithelial cell proliferation and barrier function by targeting EIF4G2. The goal of this study was to find a potential target for treating I/R injury in the intestine, as well as to prevent and mitigate the damage caused.

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Section: Discussionmentioning

confidence: 99%

miR-379-5P INHIBITION ENHANCES INTESTINAL EPITHELIAL PROLIFERATION AND BARRIER FUNCTION RECOVERY AFTER ISCHEMIA/REPERFUSION BY TARGETING EIF4G2

Jia,

Wang,

Gao

et al. 2023

Shock

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“…In addition to their roles in epigenetic and transcriptional regulation, lncRNAs also handle post-transcriptional regulation through several approaches, including the formation of specific lncRNA-protein complexes (lncRNPs) that operate as competitive endogenous RNAs (ceRNAs) or “sponges” of microRNAs (miRNAs), thereby regulating alternative splicing, mRNA degradation and diminishing mRNA stability ( 93 – 97 ). Furthermore, lncRNAs regulate several other aspects of gene expression, such as the disruption of translational processes by binding to eukaryotic translation initiation factor 4 gamma 2 (EIF4G2) and post-translational regulation via protein interactions ( 98 , 99 ).…”

Section: Lncrna Biologymentioning

confidence: 99%

LncRNA H19: a novel player in the regulation of diabetic kidney disease

Wu,

Huang

2023

Front. Endocrinol.

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Diabetic kidney disease (DKD), one of the most severe complications of diabetes mellitus (DM), has received considerable attention owing to its increasing prevalence and contribution to chronic kidney disease (CKD) and end-stage kidney disease (ESRD). However, the use of drugs targeting DKD remains limited. Recent data suggest that long non-coding RNAs (lncRNAs) play a vital role in the development of DKD. The lncRNA H19 is the first imprinted gene, which is expressed in the embryo and down-regulated at birth, and its role in tumors has long been a subject of controversy, however, in recent years, it has received increasing attention in kidney disease. The LncRNA H19 is engaged in the pathological progression of DKD, including glomerulosclerosis and tubulointerstitial fibrosis via the induction of inflammatory responses, apoptosis, ferroptosis, pyroptosis, autophagy, and oxidative damage. In this review, we highlight the most recent research on the molecular mechanism and regulatory forms of lncRNA H19 in DKD, including epigenetic, post-transcriptional, and post-translational regulation, providing a new predictive marker and therapeutic target for the management of DKD.

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“…The prepared insert was positioned in the lower compartment containing the medium (500 μL). Non-invading cells were removed after 24 hours of culture, and the quantity of invasive cells was counted after staining with 0.1% crystal violet [23].…”

Section: Transwell Invasion Assaymentioning

confidence: 99%

MAGI2 antisense RNA 3 (MAGI2-AS3) knockdown contributes to prostate cancer by downregulating proline-rich membrane anchor 1 (PRIMA1) via miR-142-3p

Lai

Huang

Li³

et al. 2023

Arch Med Sci

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IntroductionLong non-coding RNA Membrane-Associated Guanylate Kinase Inverted 2 Antisense RNA 3 (MAGI2-AS3) has been identified as a predictive characteristic for prostate cancer (PC). However, the underlying mechanism of MAGI2-AS3 in PC is yet unclear.Material and methodsThe gene expression was detected via reverse transcription quantitative PCR. Cell viability, apoptosis and invasion were detected via cell counting kit-8, caspase-3 activity, flow cytometry, and transwell assays. Tumor xenograft experiment was performed to measure the tumor growth in vivo. Luciferase and radioimmunoprecipitation assays were utilized to determine the association between microRNA (miR)-142-3p and MAGI2-AS3 or proline-rich membrane anchor 1 (PRIMA1).ResultsMAGI2-AS3 and PRIMA1 were established to be downregulated in PC, whereas miR-142-3p exhibited the upregulation in PC. In vitro and in vivo loss-of-function assays demonstrated that MAGI2-AS3 silencing increased the viability and invasiveness, enhanced the tumor growth of PC cells, while reducing apoptosis. PRIMA1 silencing in PC cells showed the similar effect as MAGI2-AS3 silencing. Moreover, the miR-142-3p inhibitor reversed the impacts of the downregulation of MAGI2-AS3 or PRIMA1 on the malignant behavior of PC cells.ConclusionsMAGI2-AS3 knockdown enhanced the malignant behavior of PC cells by targeting miR-142-3p to suppress PRIMA1 expression. Our findings reveal that MAGI2-AS3 can be a promising therapeutic target for the treatment of PC.

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Long non-coding RNA (LncRNA) SNHG7/ Eukaryotic translation initiation factor 4 gamma 2 (EIF4G2) involves in the malignant events of ovarian cancer cells with paclitaxel resistant

Cited by 7 publications

References 28 publications

miR-379-5P INHIBITION ENHANCES INTESTINAL EPITHELIAL PROLIFERATION AND BARRIER FUNCTION RECOVERY AFTER ISCHEMIA/REPERFUSION BY TARGETING EIF4G2

miR-379-5P INHIBITION ENHANCES INTESTINAL EPITHELIAL PROLIFERATION AND BARRIER FUNCTION RECOVERY AFTER ISCHEMIA/REPERFUSION BY TARGETING EIF4G2

LncRNA H19: a novel player in the regulation of diabetic kidney disease

MAGI2 antisense RNA 3 (MAGI2-AS3) knockdown contributes to prostate cancer by downregulating proline-rich membrane anchor 1 (PRIMA1) via miR-142-3p

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