CircRNA Cdr1as functions as a competitive endogenous RNA to promote hepatocellular carcinoma progression

Su, Yang; Lv, Xiurui; Yin, Wei; Zhou, Lingling; Hu, Yilin; Zhou, Ang; Qi, Fuzhen

doi:10.18632/aging.102312

Cited by 174 publications

(124 citation statements)

References 57 publications

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“…Cancer cachexia results in functional impairment, decreased physical ability and it is associated with a poor prognosis (89). The same mechanisms have been reported in other studies (90,91). It can be concluded from the aforementioned studies that exosomes can directly transfer circRNAs from cancer cells to surrounding cells, and then further mediate the biological functions of recipient cells.…”

Section: Exosomes Containing Circrnas Function In Promoting or Inhibisupporting

confidence: 54%

Exosomal circular RNA sorting mechanisms and their function in promoting or inhibiting cancer (Review)

et al. 2020

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Exosomes are nanoscale phospholipid bilayer vesicles that can be artificially engineered into vectors for the treatment of cancer. Circular RNA (circRNA), a type of non-coding RNA, has crucial regulatory functions in various aspects of cancer, such as tumorigenesis, apoptosis, proliferation, invasion, metastasis and chemo-and radiotherapeutic resistance, as well as in cancer prognosis. Notably, the exosomal transfer of circRNAs may function to both promote and inhibit cancer. Numerous studies have addressed the importance of circRNAs in cancer and non-coding RNAs (such as microRNAs and long non-coding RNAs) in exosomes. However, little research has focussed on a class of RNAs called exosomal circRNAs. The present review discusses current studies regarding exosomal circRNAs, including their biogenesis and biological functions, their abundance in exosomes and possible sorting mechanisms and their potential roles in both promoting and inhibiting cancer. It is predicted that in the next five years there will be increasing research exploring the functional mechanisms of exosomal circRNA in various diseases, in particular their roles in cancer genesis and progression.

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Section: Exosomes Containing Circrnas Function In Promoting or Inhibisupporting

confidence: 54%

Exosomal circular RNA sorting mechanisms and their function in promoting or inhibiting cancer (Review)

et al. 2020

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“…25 Inversely, Su et al pronounce that circ_CDR1as is highly expressed in HCC cells and tissues, and gain of circ_CDR1as largely promotes HCC cells to proliferate and metastasize, as well as accelerates HCC progression, highlighting its oncogenic role. 11 What is more, Xu et al point out that the expression level of circ_CDR1as in HCC and matched non-tumor tissues is comparable. 26 From our data, we also discover that circ_CDR1as expression is significantly upregulated in HCC tissues and cells.…”

Section: Discussionmentioning

confidence: 99%

“…In this work, we observe that deficiency of circ_CDR1as represses HCC cell proliferation and metastasis in vitro, as well as tumor growth in vivo, in consistent with a former paper. 11 According to the competing endogenous RNA (ceRNA) hypothesis, circRNA could act as ceRNA to sponge miRNA to exert its regulatory potency in human cancer development.…”

Section: Discussionmentioning

confidence: 99%

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<p>CircRNA CDR1as/miR-1287/Raf1 Axis Modulates Hepatocellular Carcinoma Progression Through MEK/ERK Pathway</p>

Zhang¹,

Li²,

Zhu³

et al. 2020

CMAR

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Background: Hepatocellular carcinoma (HCC) is a common lethal malignant tumor worldwide. Circular RNAs (circRNAs) have been reported to affect the development of human cancers, including HCC. In this project, we aim to clarify the functional effect of circular CDR1as (circ_CDR1as) on HCC progression. Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) or Western blot is implemented to detect the expression of circ_CDR1as, microRNA (miR)-1287 and Raf-1 proto-oncogene, serine/threonine kinase (Raf1). Cell proliferation is assessed via colony formation and 3-(4, 5)-dimethylthiazole-2-y1)-2, 5-biphenyl tetrazolium bromide (MTT) assays. Cell migration and invasion are measured by Transwell assay. The target relationship between miR-1287 and circ_CDR1as or Raf1 is validated through dual-luciferase reporter assay. The levels of epithelia-mesenchymal transition (EMT) markers and the MEK/ERK signal pathway-related proteins are examined by Western blot. Model in nude mice is constructed to determine the role of circ_CDR1as in vivo. Results: Expression of circ_CDR1as and Raf1 is elevated, while miR-1287 expression is decreased in HCC. Depletion of circ_CDR1as or Raf1 could inhibit proliferation and metastasis of HCC cells. Besides, circ_CDR1as regulates Raf1 expression by targeting miR-1287. MiR-1287 upregulation or Raf1 depletion could partially counterbalance circ_CDR1as depletion-mediated inhibitory effects on HCC cell behaviors. Moreover, circ_CDR1as depletion represses HCC progression through inactivating MEK/ERK pathway. In addition, circ_CDR1as depletion suppresses tumor growth in vivo via regulating miR-1287/Raf1 pathway. Conclusion: Circ_CDR1as depletion inhibits HCC cell proliferation and metastasis by miR-1287/Raf1 and MEK/ERK pathways, highlighting a promising molecular target for HCC treatment.

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“…CDR1as could promote the expression of AFP by sponging miR-1270. And exosomes extracted from CDR1as-overexpressed HCC cells increased proliferation and migration of surrounding normal cells (2). Knockdown of CDR1as speci cally triggered low-dose Diosbulbin-B (DB) induced GC cell death by regulating miR-7-5p/REGγ axis (3).…”

Section: Introductionmentioning

confidence: 99%

CircRNA CDR1as Promotes Glioma Progression by Regulating miR-514a-3p/STAT3 Signaling Pathway

Cao

Yang

et al. 2020

Preprint

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Background The pathogenesis of glioma is very complicated and the molecular mechanisms have not been clearly demonstrated so far. CircRNA CDR1as as non-coding RNA was highly expressed in multiple human cancers and promoted tumorigenesis and cancer progression. However, there were no reports to address the roles of CDR1as in glioma.Methods In this study, we used glioma cell lines to investigate the function of CDR1as. Cell viability, colony formation, migration, invasion, gene expression, luciferase activity, miRNA-circRNA interaction, protein-circRNA interaction, and tumor formation in vivo were assessed.Results We found that CDR1as is up-regulated in human glioma tissues and cell lines, and its expression is significantly associated with the prognosis of patients with glioma. Loss-of-function studies revealed that CDR1as increases glioma cell proliferation, migration, and invasion in vitro and tumor growth in vivo. We showed that CDR1as can bind miR-514a-3p and act as a sponge of miR-514a-3p. Furthermore, we identified that the expression of STAT3 is regulated by miR-514a-3p and CDR1as as the direct target of miR-514a-3p. Additionally, the decreased glioma cell malignancy by CDR1as knockdown can be reversed by miR-514a-3p inhibitor and overexpression of STAT3. CDR1as knockdown can result in the down-regulated expression of PCNA, Ki67, N-cadherin, and MMP9 and up-regulated expression of E-cadherin. Moreover, the aberrant expression of these genes by CDR1as knockdown also can be reversed by miR-514a-3p inhibitor and overexpression of STAT3.Conclusions Taken together, our findings uncover the molecular mechanisms of CDR1as-mediated the progression of glioma through the miR-514a-3p/STAT3 signaling pathway. These results will provide a theoretical basis for further understanding of the molecular mechanisms of glioma tumorigenesis and developing new therapeutic targets.

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CircRNA Cdr1as functions as a competitive endogenous RNA to promote hepatocellular carcinoma progression

Cited by 174 publications

References 57 publications

Exosomal circular RNA sorting mechanisms and their function in promoting or inhibiting cancer (Review)

Exosomal circular RNA sorting mechanisms and their function in promoting or inhibiting cancer (Review)

<p>CircRNA CDR1as/miR-1287/Raf1 Axis Modulates Hepatocellular Carcinoma Progression Through MEK/ERK Pathway</p>

CircRNA CDR1as Promotes Glioma Progression by Regulating miR-514a-3p/STAT3 Signaling Pathway

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