Circ_0084927 promotes cervical carcinogenesis by sponging miR-1179 that suppresses CDK2, a cell cycle-related gene

Qu, Xinhua; Zhu, Liumei; Song, Linlin; Liu, Shaohua

doi:10.21203/rs.3.rs-24972/v1

Cited by 3 publications

(3 citation statements)

References 44 publications

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“…Previous studies have shown that the expression levels of CDK2, CDK4 and CDK6 are often upregulated in various types of cancer, and are associated with tumorigenesis by interacting with other proteins (22,23). For example, Qu et al (24) reported that CDK2 served a key role in circular RNA (circ)_0084927/microRNA (miR)-1179 signaling axis-mediated cervical cancer development. Zhao et al (25) found that CDK6 knockdown suppressed gastric cancer cell proliferation via regulating the cell cycle.…”

Section: Discussionmentioning

confidence: 99%

MEX3A knockdown inhibits the tumorigenesis of colorectal cancer via modulating CDK2 expression

Zhou

et al. 2021

Exp Ther Med

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Colorectal cancer (CRC) is a malignant tumor of the gastrointestinal tract and a leading cause of cancer-associated mortality worldwide. Mex-3 RNA binding family member A (MEX3A) promotes the progression of multiple types of cancer, including ovarian and cervical cancer. However, to the best of our knowledge, the role of MEX3A in CRC is not completely understood. Therefore, the present study aimed to investigate the function of MEX3A in CRC. The mRNA and protein expression levels of MEX3A in CRC cells were analyzed using reverse transcription-quantitative PCR and western blotting, respectively. Cell Counting Kit-8 assays were used to measure cell viability. Cell apoptosis and cell cycle distribution were detected via flow cytometry, and CRC cell invasion was analyzed by performing Transwell assays. Moreover, the mitochondrial membrane potential in CRC cells was measured via JC-1 staining. The results of the present study revealed that the expression levels of MEX3A were upregulated in CRC tissues compared with adjacent healthy tissues. MEX3A knockdown notably inhibited CRC cell viability, and induced apoptosis and mitochondrial injury. In addition, MEX3A knockdown markedly induced G 1 phase cell cycle arrest in CRC cells via downregulating CDK2 expression. In conclusion, the findings of the present study suggested that MEX3A knockdown may inhibit the tumorigenesis of CRC cells by regulating CDK2 expression. Therefore, MEX3A may serve as a novel target for CRC treatment.

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Section: Discussionmentioning

confidence: 99%

MEX3A knockdown inhibits the tumorigenesis of colorectal cancer via modulating CDK2 expression

Zhou

et al. 2021

Exp Ther Med

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“…In CC, numerous circRNAs have been considered to be oncogenic drivers [15]. For instance, circ_0084927 regulated the development of CC via miR-1179/CDK2 axis [16], and circ_0000745 promoted CC cell proliferation and inhibits cell apoptosis by miR-409-3p/ATF1 axis [17]. In this study, compared with the relative normal tissues and cells, circ_0002762 was up-regulated in human CC tissues and cell lines.…”

Section: Discussionmentioning

confidence: 83%

Circ_0002762 Accelerates Glycolysis Metabolism to Promote Cervical Cancer Progression via the miR-526b-5p/HK2 Axis

Nian

Ling

Chen

2022

Gynecol Obstet Invest

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Objectives: The purpose of this study was to investigate the role and mechanism of circ_0002762 in CC. Design:Silencing circ_0002762 in CC cells and xenograft tumor models to investigate the role of circ_0002762 in CC in vitro and in vivo. Materials and Methods: The relative expression levels of circ_0002762, miR-526b-5p and hexokinase2 (HK2) in CC tissues and cells were detected by real-time quantitative polymerase chain reaction (RT-qPCR) or western blot. Glycolysis-related extracellular acidification rate, glucose production, lactic acid consumption, and ATP levels were measured using the appropriate kits. Cell proliferation was assessed by 5-Ethynyl-2'-deoxyuridine (EdU) and colony formation assay. Cell apoptosis was detected by flow cytometry. The binding relationship between miR-526b-5p and circ_0002762 or HK2 was verified by dual-luciferase reporter assay and RNA pull-down assay. Tumor growth in vivo was detected by xenograft tumor model. Results: The expressions of circ_0002762 and HK2 were up-regulated and miR-526b-5p was down-regulated in CC tissues and cells. Circ_0002762 knockdown inhibited glycolysis and proliferation and promoted apoptosis of CC cells. In addition, miR-526b-5p suppression reversed the inhibition of CC development induced by circ_0002762 silencing. HK2 overexpression eliminated the inhibition of miR-526b-5p on CC progression. Moreover, silencing of circ_0002762 inhibited CC tumor growth in vivo. Limitations:The practical application of Circ_0002762 in clinical needs further investigation. Conclusion: Circ_0002762 knockdown inhibited CC progression by regulating miR-526b-5p/HK2 axis, suggesting that circ_0002762 was a promising therapeutic strategy for CC.

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“…Other studies have shown up-regulation of a number of CDK2-interactiong circRNAs such as hsa_circ_0000520 [128], circ_0084927 [129] and circZFR [130] in cervical cancer patients. Notably, up-regulation of circZFR has been associated with lymphatic metastasis in this type of cancer [130].…”

Section: Investigations In Clinical Samplesmentioning

confidence: 92%

A review on the role of cyclin dependent kinases in cancers

et al. 2022

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The Cyclin-dependent kinase (CDK) class of serine/threonine kinases has crucial roles in the regulation of cell cycle transition and is mainly involved in the pathogenesis of cancers. The expression of CDKs is controlled by a complex regulatory network comprised of genetic and epigenetic mechanisms, which are dysregulated during the progression of cancer. The abnormal activation of CDKs results in uncontrolled cancer cell proliferation and the induction of cancer stem cell characteristics. The levels of CDKs can be utilized to predict the prognosis and treatment response of cancer patients, and further understanding of the function and underlying mechanisms of CDKs in human tumors would pave the way for future cancer therapies that effectively target CDKs. Defects in the regulation of cell cycle and mutations in the genes coding cell-cycle regulatory proteins lead to unrestrained proliferation of cells leading to formation of tumors. A number of treatment modalities have been designed to combat dysregulation of cell cycle through affecting expression or activity of CDKs. However, effective application of these methods in the clinical settings requires recognition of the role of CDKs in the progression of each type of cancer, their partners, their interactions with signaling pathways and the effects of suppression of these kinases on malignant features. Thus, we designed this literature search to summarize these findings at cellular level, as well as in vivo and clinical levels.

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Circ_0084927 promotes cervical carcinogenesis by sponging miR-1179 that suppresses CDK2, a cell cycle-related gene

Cited by 3 publications

References 44 publications

MEX3A knockdown inhibits the tumorigenesis of colorectal cancer via modulating CDK2 expression

MEX3A knockdown inhibits the tumorigenesis of colorectal cancer via modulating CDK2 expression

Circ_0002762 Accelerates Glycolysis Metabolism to Promote Cervical Cancer Progression via the miR-526b-5p/HK2 Axis

A review on the role of cyclin dependent kinases in cancers

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