miR-107 targets cyclin-dependent kinase 6 expression, induces cell cycle G1 arrest and inhibits invasion in gastric cancer cells

Li, Feng; Xie, Yun; Zhang, Hao; Wu, Yun

doi:10.1007/s12032-011-9823-1

Cited by 110 publications

(93 citation statements)

References 16 publications

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“…They found that the nodal metastasis of endocervical adenocarcinomas is positively associated with the high frequencies of copy number amplification in CDK6 (Hirai et al, 2004). Moreover, suppression of CDK6 can inhibit cell invasion of gastric cancer cells (Feng et al, 2012), which is consistent with our results of cell migration and invasion experiments, despite the accurate mechanisms are still unknown. Taken together, we interpret these results to indicate that let-7a induced downregulation of CDK6, as manifested by subsequent modulation of the expression of its target gene, to impact ES cell growth and metastasis.…”

Section: Discussionsupporting

confidence: 84%

Retracted: Let-7a Functions as a Tumor Suppressor in Ewing's Sarcoma Cell Lines Partly by Targeting Cyclin-Dependent Kinase 6

Zhang

Yu²,

Chen³

et al. 2014

DNA and Cell Biology

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MicroRNAs play an important role in the development and progression of Ewing's sarcoma (ES). Especially, the expression of let-7a has been reported to be significantly downregulated in various cancers, and can affect the initiation and maintenance of tumor progression. However, the relative effects of let-7a on ES cells and relative mechanisms are largely unknown. In this study, we identified the underexpression of let-7a in human ES cells comparing with the human mesenchymal stem cells. Then, we sought to compensate for its loss through exogenous transfection with let-7a mimic into ES cell lines A673 and SK-ES-1. Restored let-7a expression inhibited cell proliferation, migration, as well as invasion; arrested cell cycle progression; and induced cell apoptosis of both cell lines. Moreover, bioinformatic prediction suggested that cyclin-dependent kinase 6 (CDK6), which is overexpressed and functions as an oncoprotein in ES cells, is a putative target gene of let-7a. Using mRNA and protein expression analysis and luciferase assays, we further identified the target role of CDK6. Finally, we found that restored CDK6 expression in ES cells that had been treated with let-7a mimic before could partly dampen let-7a-mediated tumor suppression. Taken together, our results showed that let-7a acted as a tumor suppressor in ES by targeting CDK6, and it may provide novel diagnostic and therapeutic options for human Ewing sarcoma clinical operation in future.

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Section: Discussionsupporting

confidence: 84%

Retracted: Let-7a Functions as a Tumor Suppressor in Ewing's Sarcoma Cell Lines Partly by Targeting Cyclin-Dependent Kinase 6

Zhang

Yu²,

Chen³

et al. 2014

DNA and Cell Biology

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“…Interestingly, we identified a group of miRNAs transiently upregulated in the early days of muscle regeneration (cluster C, Fig. 2B) including cell cycle-related miR-34c, -107, and -292 (2,18,34). The miR-34 family of miRNAs have been repeatedly implicated as important regulators of the cell cycle and are directly induced by p53 (24).…”

Section: Discussionmentioning

confidence: 94%

MiR-351 transiently increases during muscle regeneration and promotes progenitor cell proliferation and survival upon differentiation

Chen

Melton

Gelfond

et al. 2012

Physiological Genomics

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Chen Y, Melton DW, Gelfond JAL, McManus LM, Shireman PK. MiR-351 transiently increases during muscle regeneration and promotes progenitor cell proliferation and survival upon differentiation. Physiol Genomics 44: 1042-1051, 2012. First published September 11, 2012; doi:10.1152/physiolgenomics.00052.2012.-MicroRNAs (miRNAs) regulate many biological processes including muscle development. However, little is known regarding miRNA regulation of muscle regeneration. Murine tibialis anterior muscle was evaluated after cardiotoxin-induced injury and used for global miRNA expression analysis. From day 1 through day 21 following injury, 298 miRNAs were significantly changed at least at one time point, including 86 miRNAs that were altered Ͼ10-fold compared with uninjured skeletal muscle. Temporal miRNA expression patterns included inflammation-related miRNAs (miR-223 and -147) that increased immediately after injury; this pattern contrasted to that of mature muscle-specific miRNAs (miR-1, -133a, and -499) that abruptly decreased following injury followed by upregulation in later regenerative events. Another cluster of miRNAs were transiently increased in the early days of muscle regeneration including miR-351, a miRNA that was also transiently expressed during myogenic progenitor cell (MPC) differentiation in vitro. Based on computational predictions, further studies demonstrated that E2f3 was a target of miR-351 in myoblasts. Moreover, knockdown of miR-351 expression inhibited MPC proliferation and promoted apoptosis during MPC differentiation, whereas miR-351 overexpression protected MPC from apoptosis during differentiation. Collectively, these observations suggest that miR-351 is involved in both the maintenance of MPC proliferation and the transition into differentiated myotubes. Thus, a novel, timedependent sequence of molecular events during muscle regeneration has been identified; miR-351 inhibits E2f3 expression, a key regulator of cell cycle progression and proliferation, and promotes MPC proliferation and protects early differentiating MPC from apoptosis, important events in the hostile tissue environment after acute muscle injury.microRNA; myogenic progenitor cell; muscle regeneration; muscle differentiation SKELETAL MUSCLES ARE DAMAGED and repaired repeatedly throughout life. The capacity for skeletal muscle growth and regeneration is conferred by satellite cells located between the basal lamina and the sarcolemma of mature myofibers (21). Upon injury, satellite cells reenter the cell cycle, proliferate, and then exit the cell cycle either to renew the quiescent satellite cell pool or to differentiate into mature myofibers (1). Despite recent advances, genes involved in these processes are still largely unknown. Understanding the molecular mechanisms that regulate satellite cell activities could promote development of novel countermeasures to enhance muscle regeneration that is compromised by diseases or aging.Both cell proliferation and differentiation programs are essential for muscle regeneration. The dec...

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“…One example is cyclin D1, which is regulated by miR449a [35] , miR-193b [36] , miR-15/16 [37][38][39] , miR-19a [40] , miR-195 [41] , and miR-302a [42] . The cyclin D1 binding proteins CDK4 and CDK6 are also regulated by a number of miRNAs, including miR-107 [43] , miR-449a [44] , miR-129 [45] , miR-125b [46] , miR-15/16 [39] , miR-24 [47] , miR-195 [41] , and miR-124a [48] . Another important G 1 /S regulator cyclin E, is down-regulated by miR-16 [37] and miR-195 [49] .…”

Section: Mir-34 Familymentioning

confidence: 99%

Macro-management of microRNAs in cell cycle progression of tumor cells and its implications in anti-cancer therapy

Liang

2011

Acta Pharmacol Sin

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The cell cycle, which is precisely controlled by a number of regulators, including cyclins and cyclin-dependent kinases (CDKs), is crucial for the life cycle of mammals. Cell cycle dysregulation is implicated in many diseases, including cancer. Recently, compelling evidence has been found that microRNAs play important roles in the regulation of cell cycle progression by modulating the expression of cyclins, CDKs and other cell cycle regulators. Herein, the recent findings on the regulation of the cell cycle by microRNAs are summarized, and the potential implications of miRNAs in anti-cancer therapies are discussed.

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miR-107 targets cyclin-dependent kinase 6 expression, induces cell cycle G1 arrest and inhibits invasion in gastric cancer cells

Cited by 110 publications

References 16 publications

Retracted: Let-7a Functions as a Tumor Suppressor in Ewing's Sarcoma Cell Lines Partly by Targeting Cyclin-Dependent Kinase 6

Retracted: Let-7a Functions as a Tumor Suppressor in Ewing's Sarcoma Cell Lines Partly by Targeting Cyclin-Dependent Kinase 6

MiR-351 transiently increases during muscle regeneration and promotes progenitor cell proliferation and survival upon differentiation

Macro-management of microRNAs in cell cycle progression of tumor cells and its implications in anti-cancer therapy

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