Upregulation of circ-0000745 in acute lymphoblastic leukemia enhanced cell proliferation by activating ERK pathway

Liu, Xiaoliu; Zhou, Changjiang; Li, Yongjian; Deng, Yurong; Lu, Wensheng; Li, Juan

doi:10.1016/j.gene.2020.144726

Cited by 26 publications

(23 citation statements)

References 19 publications

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“…H-Ras activation promotes invasion in cutaneous squamous cell carcinoma (64).RAF1 rearrangements are common in pancreatic acinar cell carcinomas(65). MEK1/2 inhibitors suppresses cancer growth in mice (66) and circ-0000745 enhanced cerll proliferation by activating ERK pathway (67). C-jun is activated in renal cell carcinoma (68).…”

Section: Discussionmentioning

confidence: 99%

miR155 Enhances Autophagy by Reducing MBD5 and METTL3 in Human Liver Cancer Stem Cells

Lu¹,

Chen²,

Xin³

et al. 2020

Preprint

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Background: miR-155 is a widely reported carcinogenic miRNA, with up-regulated expression in a variety of human cancers. Methods: Liver cancer stem cells were isolated from Huh7 cells; gene infection, RT-PCR, Western blotting and tumorigenesis test in vitro and in vivo were performed to analyze the signaling pathway. Results: we demonstrate that miR-155 inhibits the expression of MBD5 and METTL3 , reducing the expression of DNMT1. In particular, miR155 inhibits the interaction between MBD5 and DNMT1, thereby inhibiting the binding capacity among MBD5, DNMT1 and IGFII (H19 ICR, IGFII DMR, IGFII Enhancer) DNA, inhibiting IGFII DNA methylation modification. Importantly, miR-155 promotes the formation of DNA loops in the IGFII DNA region (H19 ICR-IGFII Enhancer, IGFII DMR-IGFII Enhancer). Therefore, miR155 promotes the binding ability of H19-pre miR675 to histone methyltransferases SUV39h2 dependent on the H19 ICR-IGFII enhancer DNA loop and enhances the methylation modification of histone H3 on the ninth lysine . Then, the binding ability of RNA polII to P300 was enhanced by the formation of H3K9me2-RNA polII-P300 complex. Furthermore, miR155 promotes the binding ability of the RNA PolII-P300 complex to the IGFII promoter dependent on the IGFII DMR-IGFII enhancer DNA loop and promotes the expression of IGFII. Further research shows that miR155 promotes the binding of IGFII to stemness factors and the loading of stemness factors into the promoter region of HGF, which promotes the expression of hepatocyte growth factor HGF. In particular, miR155 promotes the expression of albumin gene (ALB) via HGF-c-MET, and then promotes the Sirt1 expression through ALB. Strikingly, miR155 promotes the autophagy dependent on acetylase Sirt1,including that miR155 promotes LC3 activation dependent on acetylase sirt1 and enhances binding capacity of LC3 to TP53INP2 / DOR, ATG4, ATG3 and ATG7, and the binding ability of the interaction between ATG5, ATG12, ATG6L1, ATG9. More meaningfully, miR155 enhances the ability of H-Ras to bind to the autophagosomes Beclin1, vps34, vps5, Uvrage, bif1, Lamp1, Lamp2, Lamp3, Rubicon, Rab24 dependent on autophagy, thereby enhancing the expression of H-Ras. Furthermore, miR155 enhances the expression of pRaf1, pMEK1 / 2, pERK1 / 2, pElK, pJak, Jun, pAKT, pmTOR, P70S6K, 4E-BP1, SGK1, C-myc dependent on H-Ras.Finally, miR-155 promotes the malignant growth of human liver cancer stem cells mediated by H-Ras.Conclusions: these results provide a valuable theoretical basis for therapeutic targets of liver cancer based on miR-155.

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Section: Discussionmentioning

confidence: 99%

miR155 Enhances Autophagy by Reducing MBD5 and METTL3 in Human Liver Cancer Stem Cells

Lu¹,

Chen²,

Xin³

et al. 2020

Preprint

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“…GC: gastric cancer; CRC: colorectal cancer; PC: pancreatic cancer; HCC: hepatocellular carcinoma; BC: breast cancer; CC: cervical cancer; OC: ovarian cancer; EC: endometrial cancer; NSCLC: non-small cell lung cancer; LUAD: lung adenocarcinoma; NPC: nasopharyngeal carcinoma; BCa: bladder cancer; PCa: prostate cancer; RCC: renal cell carcinoma; UC: urothelial carcinoma; GBM: glioblastoma; TC: thyroid carcinoma; OS: osteosarcoma; RMS: rhabdomyosarcoma leukemia (ALL) cells by declining the expression of c-Myc and Bcl-2 [27]. Upregulation of circ-0000745 resulted in enhanced proliferation of ALL cells by activating ERK [28]. Transcriptomic sequencing of 21 de novo chronic lymphocytic leukemia (CLL) patients revealed differentially expression of 859 circRNAs distinguished CLL cells from normal B cells [29].…”

Section: Facilitating Tumorigenesis Of Hematological Malignanciesmentioning

confidence: 99%

“…In terms of lymphocytic leukemia, knockdown of circPVT1 accelerated the apoptosis of acute lymphocytic leukemia (ALL) cells by declining the expression of c-Myc and Bcl-2 [ 27 ]. Upregulation of circ-0000745 resulted in enhanced proliferation of ALL cells by activating ERK [ 28 ]. Transcriptomic sequencing of 21 de novo chronic lymphocytic leukemia (CLL) patients revealed differentially expression of 859 circRNAs distinguished CLL cells from normal B cells [ 29 ].…”

Section: Functions Of Circrnas In Hematological Malignanciesmentioning

confidence: 99%

The functions and clinical significance of circRNAs in hematological malignancies

et al. 2020

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With covalently closed circular structures, circular RNAs (circRNAs) were once misinterpreted as by-products of mRNA splicing. Being abundant, stable, highly conserved, and tissue-specific, circRNAs are recently identified as a type of regulatory RNAs. CircRNAs bind to certain miRNAs or proteins to participate in gene transcription and translation. Emerging evidence has indicated that the dysregulation of circRNAs is closely linked to the tumorigenesis and treatment response of hematological malignancies. CircRNAs play critical roles in various biological processes, including tumorigenesis, drug resistance, tumor metabolism, autophagy, pyroptosis, and ferroptosis. The N6-methyladenosine modification of circRNAs and discovery of fusion-circRNAs provide novel insights into the functions of circRNAs. Targeting circRNAs in hematological malignancies will be an attractive treatment strategy. In this review, we systematically summarize recent advances toward the novel functions and molecular mechanisms of circRNAs in hematological malignancies, and highlight the potential clinical applications of circRNAs as novel biomarkers and therapeutic targets for future exploration.

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“…Silencing circPVT1 repressed ALL cell proliferation and induced apoptosis through inhibiting c‐Myc and Bcl‐2 protein expression 58 . Furthermore, circ‐0000745 is reported to be up‐regulated in ALL cells, which promotes leukemia cell proliferation through increasing the activity of ERK1/2 59 . In addition, circRNAs produced from genes related to ALL and B‐cell differentiation (JAK2, PAX5, IKZF1, ETV6, and EBF1) are abundantly expressed in hyperdiploid leukemia compared with normal leukocytes 60 …”

Section: Circrnas In Leukemiamentioning

confidence: 99%

Recent progress in study of circRNAs and its role in leukemia

Tang

Sun

et al. 2020

Journal of Leukocyte Biology

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Circular RNAs (circRNAs) are a class of newly identified noncoding RNA and are considered as a new feature of eukaryotic gene expression. Hundreds of thousands of endogenous circRNAs have been found in mammalian cells, which we knew little before. CircRNAs are covalently closed, circular RNA molecules that typically comprise exonic sequences and are spliced at canonical splice sites. Researchers with RNA-Seq technology have identified that the expression of circR-NAs is developmentally regulated, tissue-and cell-type specific. Like long noncoding RNAs (lncR-NAs), circRNAs are becoming a new research hotspot in the RNA field, and aberrant expression of circRNAs could contribute to carcinogenesis. Recent studies have demonstrated that circRNAs play important roles in the development, maintenance, and progression of leukemia. Herein, we describe the biologic characteristics and functions of circRNAs, with a focus on circRNAs that play essential roles in leukemia.

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Upregulation of circ-0000745 in acute lymphoblastic leukemia enhanced cell proliferation by activating ERK pathway

Cited by 26 publications

References 19 publications

miR155 Enhances Autophagy by Reducing MBD5 and METTL3 in Human Liver Cancer Stem Cells

miR155 Enhances Autophagy by Reducing MBD5 and METTL3 in Human Liver Cancer Stem Cells

The functions and clinical significance of circRNAs in hematological malignancies

Recent progress in study of circRNAs and its role in leukemia

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