MicroRNA-133b is a key promoter of cervical carcinoma development through the activation of the ERK and AKT1 pathways

Qin, Wenyan; Dong, Ping; Ma, Cailing; Mitchelson, Keith; Deng, Tuo; Zhang, L; Sun, Yimin; Feng, Xiaoli; Ding, Yan; Lü, Xiaomei; He, Jie; Wen, Hao; Cheng, Jing

doi:10.1038/onc.2011.561

Cited by 111 publications

(90 citation statements)

References 41 publications

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“…Note that the changed level of myomiR typically contributes to cancer progression. Reduced levels of a single myomiR are associated with PDAC [103] , NSCLC [105] and HCC [98] , whilst an elevated single miR is associated with cervical carcinoma [121] and bladder cancer (TCC) [122] . Increased expression of miR-1/-133a is associated with t(14;16) translocation multiple myeloma [152] , whilst reduced expression is associated with prostate cancer [102] and RCC [138] , respectively.…”

Section: Myomirs and Cancermentioning

confidence: 99%

“…The expressed alleles of the myomiRs can be assessed accurately by employing pri or premiR RTPCR assays. For example, only cistron miR12/133a1 is found expressed in AML, presumably due to specific activation of that cistron [120] and amongst the myomiRs only premiR133b is elevated in cervical cancer [121] , in bladder cancer [122] , and in progressive prostate cancer [123] . We suggest that initial microarray profiling be confirmed by pri-or premiRNA assay of each miR isomer independently.…”

Section: Cancer and Downregulated Myomirsmentioning

confidence: 99%

“…In cervical cancer the upregulation of miR 133b is associated with downregulation of Mst2 protein kinase (STE20), Cdc42 and RhoA, which in turn lead to increased pERK and pAKT1 signalling activity, resulting in tumorigenesis and metastatic cancer proliferation [121] . RhoA, Cdc42 and other small Rho GTPases are components the Rho-kinase pathway which is a key controller of fundamental cellular processes such as cell motility, cell proliferation, cell division, cell differentiation, cell apoptosis, as well as morphological structure development, epithelial and skin morphogenesis, nerve system and limb development [146148] .…”

Section: Upregulated Myomirs In Cancermentioning

confidence: 99%

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Roles of the canonical myomiRs miR-1, -133 and -206 in cell development and disease

Mitchelson¹

2015

WJBC

136

132

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MicroRNAs are small non-coding RNAs that participate in different biological processes, providing subtle combinational regulation of cellular pathways, often by regulating components of signalling pathways. Aberrant expression of miRNAs is an important factor in the development and progression of disease. The canonical myomiRs (miR-1, -133 and -206) are central to the development and health of mammalian skeletal and cardiac muscles, but new findings show they have regulatory roles in the development of other mammalian non-muscle tissues, including nerve, brain structures, adipose and some specialised immunological cells. Moreover, the deregulation of myomiR expression is associated with a variety of different cancers, where typically they have tumor suppressor functions, although examples of an oncogenic role illustrate their diverse function in different cell environments. This review examines the involvement of the related myomiRs at the crossroads between cell development/ tissue regeneration/tissue inflammation responses, and cancer development. Core tip: The roles of the canonical muscle-associated microRNAs are reviewed, including microRNA families miR-1 and miR-133, and single miR-206, which are collectively known as the "myomiRs". The myomiRs act at the crossroads of the molecular regulation of muscle cells, linking between pathways for cell differentiation, development and maintenance, but also potentiate aberrant cell growth in numerous non-muscle cancers. Typically myomiRs are downregulated in cancers, but some myomiRs are upregulated in a few cancers, yet each dysregulation event advances tumor progression. The review examines normal and disease-linked molecular changes associated with the myomiRs, and collates the extensive literature into accessible tables. REVIEW

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Section: Myomirs and Cancermentioning

confidence: 99%

Section: Cancer and Downregulated Myomirsmentioning

confidence: 99%

Section: Upregulated Myomirs In Cancermentioning

confidence: 99%

See 1 more Smart Citation

Roles of the canonical myomiRs miR-1, -133 and -206 in cell development and disease

Mitchelson¹

2015

WJBC

136

132

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“…Although once considered to represent transcriptional "noise," the posttranscriptional regulator microRNAs (miRNAs) are now recognized to have crucial roles in the pathogenesis of cervical cancer based on the expression of dysreulation (11), such as miR-21, -133b, -138, and so on (12)(13)(14). Of special interest, given that over 50% of miRNAs are located at fragile sites and aberrant regions of chromosomes involved in cancer (15), breakpoint-associated miRNAs might contribute a new insight for considering the causal role of fragile sites in cancer development (16).…”

Section: Introductionmentioning

confidence: 99%

Genetic and Methylation-Induced Loss of miR-181a2/181b2 within chr9q33.3 Facilitates Tumor Growth of Cervical Cancer through the PIK3R3/Akt/FoxO Signaling Pathway

Mei

Zhang

et al. 2017

Clinical Cancer Research

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Purpose: Loss of Chr9q31-33 is one of the most common chromosome imbalances of cervical cancer, but the underlying mechanism has not been well documented.Experimental Design: The loss of heterozygosity (LOH) status of Chr9q31-33 was investigated utilizing 26 microsatellite markers. We detected the expression of miR-181a2/181b2 by qRT-PCR analysis of cervical cancer cell lines and 100 paired tumor samples and corresponding adjacent non-tumor tissues. Kaplan-Meier and Cox proportional hazard regression analyses were performed to identify the prognostic value of miR-181a2/181b2. Regulation of expression was analyzed by methylation-specific PCR. The tumorsuppressing effects of miR-181a2/181b2 were determined in vitro and in vivo. The target gene and signaling pathway that mediated the function of miR-181a2/181b2 were also identified.Results: Chr9q33.3 was identified as one of the most deleted regions in cervical cancer. Underexpression of miR-181a2/ 181b2 was detected in 46% of cervical cancer and was induced by the LOH of chr9q33.3 and promoter hypermethylation. Attenuated miR-181a2/181b2 expression predicted a poor prognostic phenotype and advanced clinical stage of cervical cancer. miR-181a2/181b2 prominently dampened cell-cycle progression, suppressed cell growth, and promoted apoptosis of tumor cells in vitro. They also effectively impeded tumor formation and growth in vivo. miR-181a2/181b2 exert the tumor suppressor ability by depressing the direct target PIK3R3 (p55g) and consequently modulating the PIK3R3/Akt/FoxO signaling pathway.Conclusions: We demonstrated a cause-and-effect event beginning from loss of chr9q33.3, a frequent event in cervical cancer, to the underexpression of miR-181a2/181b2, leading to the elevated activation of the PI3K pathway.

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“…45 In addition, the miR-133b family indirectly upregulates the Akt1 pathway during tumorigenesis. 46 The miR-9500 also suppresses metastatic activity compared with the NC or ASO-miR-9500 (Figure 8). Akt1 activation and expression results in the progression of tumorigenesis, as well as metastasis, in various cancers.…”

Section: Discussionmentioning

confidence: 95%

The novel miR-9500 regulates the proliferation and migration of human lung cancer cells by targeting Akt1

Jung

Lee

et al. 2014

Cell Death Differ

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MicroRNAs have crucial roles in lung cancer cell development. They regulate cell growth, proliferation and migration by mediating the expression of tumor suppressor genes and oncogenes. We identified and characterized the novel miR-9500 in human lung cancer cells. The miR-9500 forms a stem-loop structure and is conserved in other mammals. The expression levels of miR-9500 were reduced in lung cancer cells and lung cancer tissues compared with normal tissues, as verified by TaqMan miRNA assays. It was confirmed that the putative target gene, Akt1, was directly suppressed by miR-9500, as demonstrated by a luciferase reporter assay. The miR-9500 significantly repressed the protein expression levels of Akt1, as demonstrated via western blot, but did not affect the corresponding mRNA levels. Akt1 has an important role in lung carcinogenesis, and depletion of Akt1 has been shown to have antiproliferative and anti-migratory effects in previous studies. In the current study, the overexpression of miR-9500 inhibited cell proliferation and the expression of cell cycle-related proteins. Likewise, the overexpression of miR-9500 impeded cell migration in human lung cancer cells. In an in vivo assay, miR-9500 significantly suppressed Fluc expression compared with NC and ASO-miR-9500, suggesting that cell proliferation was inhibited in nude mice. Likewise, miR-9500 repressed tumorigenesis and metastasis by targeting Akt1. These data indicate that miR-9500 might be applicable for lung cancer therapy.

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MicroRNA-133b is a key promoter of cervical carcinoma development through the activation of the ERK and AKT1 pathways

Cited by 111 publications

References 41 publications

Roles of the canonical myomiRs miR-1, -133 and -206 in cell development and disease

Roles of the canonical myomiRs miR-1, -133 and -206 in cell development and disease

Genetic and Methylation-Induced Loss of miR-181a2/181b2 within chr9q33.3 Facilitates Tumor Growth of Cervical Cancer through the PIK3R3/Akt/FoxO Signaling Pathway

The novel miR-9500 regulates the proliferation and migration of human lung cancer cells by targeting Akt1

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