Targeted inhibition of the expression of both MCM5 and MCM7 by miRNA-214 impedes DNA replication and tumorigenesis in hepatocellular carcinoma cells

Wang, Jun; Amin, Aftab; Cheung, Man Hei; Shi, Linjing; Liang, Chun

doi:10.1016/j.canlet.2022.215677

Cited by 13 publications

(15 citation statements)

References 46 publications

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“…miR-214 is abnormally expressed in tumours of many organs, including nasopharyngeal, pulmonary, hepatic, colorectal, pancreatic, cervical, and vesical carcinomas [ 46 – 48 ]. The pathogenesis and metastasis of these tumours are closely associated with the expression of miR-214 [ 49 – 52 ].…”

Section: Discussionmentioning

confidence: 99%

“…According to the results of this experiment, there may be a feedback regulatory loop between PTEN and PI3K/AKT in renal fibrosis induced by miR-214, but this conclusion needs further experimental confirmation. miR-214 is abnormally expressed in tumours of many organs, including nasopharyngeal, pulmonary, hepatic, colorectal, pancreatic, cervical, and vesical carcinomas [46][47][48]. The pathogenesis and metastasis of these tumours are closely associated with the expression of miR-214 [49][50][51][52].…”

Section: Discussionmentioning

confidence: 99%

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Knockdown of miR-214 Alleviates Renal Interstitial Fibrosis by Targeting the Regulation of the PTEN/PI3K/AKT Signalling Pathway

Hou

Wang

et al. 2022

Oxidative Medicine and Cellular Longevity

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The microRNA-214 (miR-214) precursor is formed by the DNM3 gene on human chromosome 1q24.3, which is encoded and transcribed in the nucleus and processed into mature miR-214 in the cytoplasm. Association of miR-214 with the interstitial fibrosis of the kidney has been reported in existing research. Renal interstitial fibrosis is considered necessary during the process of various renal injuries in chronic kidney disease (CKD). One of the important mechanisms is the TGF- (transforming growth factor-) β1-stimulated epithelial interstitial transformation (EMT). The specific mechanisms of miR-214-3p in renal interstitial fibrosis and whether it participates in EMT are worthy of further investigation. In this paper, we first demonstrated modulation of the downstream PI3K/AKT axis by miR-214-3p through targeting phosphatase and tension protein homologues (PTEN), indicating the miRNA’s participation in unilateral ureteral obstruction (UUO) nephropathy and TGF-β1-induced EMT. We overexpressed or silenced miR-214-3p and PTEN for probing into the correlation of miR-214-3p with PTEN and the downstream PI3K/AKT signalling pathways. According to the results of the study, miR-214-3p overexpression silenced PTEN, activated the PI3K/AKT signalling pathway, and exacerbated EMT induced by TGF-β1, while miR-214-3p knockdown had the opposite effect. In miR-214-3p knockdown mice, the expression of PTEN was increased, the PI3K/AKT signalling pathway was inhibited, and fibrosis was alleviated. In conclusion, miR-214-3p regulates the EMT of renal tubular cells induced by TGF-β1 by targeting PTEN and regulating the PI3K/AKT signalling pathway. Furthermore, miR-214-3p knockdown can reduce renal interstitial fibrosis through the PTEN/PI3K/AKT pathway.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Knockdown of miR-214 Alleviates Renal Interstitial Fibrosis by Targeting the Regulation of the PTEN/PI3K/AKT Signalling Pathway

Hou

Wang

et al. 2022

Oxidative Medicine and Cellular Longevity

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“…Zhang et al reported that CDCA3 is regulated by miR-4677-3p during lung cancer development [60]. Four other genes involved in the ceRNA network, including MCM7 [27], NCAPG2 [28], SETD6 [31], and KIF22 [32] have also been reported to involved in lung cancer progression. These eight genes might be potential therapeutic targets in the small-cell lung cancer, which have not been studied for now.…”

Section: Discussionmentioning

confidence: 99%

“…5a-5d, 5k). We selected eight cancer-related mRNAs, including CDCA3 [25], DIAPH3 [26], MCM7 [27], NCAPG2 [14,28], TPD52 [29], PRC1 [30], SETD6 [31] and KIF22 [32], for RT-qPCR examination. Consistent with the RNA-seq results, mRNA levels of all the eight genes showed signi cant increases in SCLC tissues (Fig.…”

Section: Validation Of the Differently Expressed Lncrnas And Mrnas Re...mentioning

confidence: 99%

Identification of lncRNA, miRNA and mRNA expression profiles and ceRNA Networks in small cell lung cancer

Zhang

Zhou

Zhang

et al. 2022

Preprint

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Background Small cell lung cancer (SCLC) is a highly lethal malignant tumor. It accounts for approximately 15% of newly diagnosed lung cancers. Long non-coding RNAs (lncRNAs) can regulate gene expression and contribute to tumorigenesis through interactions with microRNAs (miRNAs). However, there are only a few studies reporting the expression profiles of lncRNAs, miRNAs, and mRNAs in SCLC. Also, the role of differentially expressed lncRNAs, miRNAs, and mRNAs in relation to competitive endogenous RNAs (ceRNA) network in SCLC remain unclear. Results In the present study, we first performed next generation sequencing (NGS) with six pairs of SCLC tumors and adjacent non-cancerous tissues obtained from SCLC patients. Overall, 29 lncRNAs, 48 miRNAs, and 510 mRNAs were found to be differentially expressed in SCLC samples (|log2[fold change] | > 1; P < 0.05). Bioinformatics analysis was performed to predict and construct a lncRNA-miRNA-mRNA ceRNA network, which included 9 lncRNAs, 11 miRNAs, and 392 mRNAs. Four up-regulated lncRNAs and related mRNAs in the ceRNA regulatory pathways were selected and validated by quantitative PCR. In addition, we examined the role of the most upregulated lncRNA, TCONS_00020615, in SCLC cells. We found that TCONS_00020615 may regulate SCLC tumorigenesis through the TCONS_00020615–hsa-miR-26b-5p–TPD52 pathway. Conclusions Taken together, our findings may help identify some potential biomarkers and therapy targets for SCLC. Also, our study may provide new evidence for the underlying regulatory mechanism in SCLC.

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“…Chromosomal DNA replication is stringently regulated to ensure that genome duplication occurs exactly once per cell cycle ( Tanaka et al, 1997 ; Zhai et al, 2010 ; Diffley, 2011 ; Zhai et al, 2011 ; Costa et al, 2013 ; Amin et al, 2019 , 2020 ; Kyei Barffour & Acheampong, 2021 ; Lin & Prasanth, 2021 ). Origins of DNA replication are marked and protected by the origin recognition complex (ORC), which forms a loading pad for the recruitment of various other DNA replication-initiation proteins to form pre-replicative complexes (pre-RCs) at replication origins during the M-to-G 1 transition ( Zhang et al, 2002 ; Chen et al, 2007 ; Lee et al, 2010 ; Ma et al, 2010 ; Huo et al, 2012 ; Huang et al, 2016b ; Cheung et al, 2019 ; Wang et al, 2022 ). The completion of pre-RC formation (also referred to as replication licensing/origin licensing) entails the loading of the head-to-head Mcm2-7p double-hexamer at origins of replication ( Evrin et al, 2009 ; Remus et al, 2009 ).…”

Section: Introductionmentioning

confidence: 99%

An essential Noc3p dimerization cycle mediates ORC double-hexamer formation in replication licensing

Amin

Khan

et al. 2023

Life Sci. Alliance

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Replication licensing, a prerequisite of DNA replication, helps to ensure once-per-cell-cycle genome duplication. Some DNA replication-initiation proteins are sequentially loaded onto replication origins to form pre-replicative complexes (pre-RCs). ORC and Noc3p bind replication origins throughout the cell cycle, providing a platform for pre-RC assembly. We previously reported that cell cycle–dependent ORC dimerization is essential for the chromatin loading of the symmetric MCM double-hexamers. Here, we usedSaccharomyces cerevisiaeseparation-of-functionNOC3mutants to confirm the separable roles of Noc3p in DNA replication and ribosome biogenesis. We also show that an essential and cell cycle–dependent Noc3p dimerization cycle regulates the ORC dimerization cycle. Noc3p dimerizes at the M-to-G1transition and de-dimerizes in S-phase. The Noc3p dimerization cycle coupled with the ORC dimerization cycle enables replication licensing, protects nascent sister replication origins after replication initiation, and prevents re-replication. This study has revealed a new mechanism of replication licensing and elucidated the molecular mechanism of Noc3p as a mediator of ORC dimerization in pre-RC formation.

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Targeted inhibition of the expression of both MCM5 and MCM7 by miRNA-214 impedes DNA replication and tumorigenesis in hepatocellular carcinoma cells

Cited by 13 publications

References 46 publications

Knockdown of miR-214 Alleviates Renal Interstitial Fibrosis by Targeting the Regulation of the PTEN/PI3K/AKT Signalling Pathway

Knockdown of miR-214 Alleviates Renal Interstitial Fibrosis by Targeting the Regulation of the PTEN/PI3K/AKT Signalling Pathway

Identification of lncRNA, miRNA and mRNA expression profiles and ceRNA Networks in small cell lung cancer

An essential Noc3p dimerization cycle mediates ORC double-hexamer formation in replication licensing

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