MiR-132, miR-15a and miR-16 synergistically inhibit pituitary tumor cell proliferation, invasion and migration by targeting Sox5

Wang, Renjie; Liang, Haiqian

doi:10.1016/j.canlet.2014.10.003

Cited by 122 publications

(92 citation statements)

References 24 publications

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“…Also, miR‐16 targets FGF2/FGFR1 directly, and phosphorylated AKT and ERK levels are reduced in cancer‐associated fibroblasts (CAFs) following miR‐16 transfection . MiR‐16 targets SOX5 while SOX5 induces EMT through transactivation of TWIST1 in breast cancer cells . An indispensable role for BMI‐1 has been shown in regulation of EMT especially in BC cells .…”

Section: Discussionmentioning

confidence: 99%

miR‐16 enhances miR‐302/367‐induced reprogramming and tumor suppression in breast cancer cells

2020

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Overexpression of either miR‐302 or miR‐302/367 cluster induces reprogramming of cancer cells and exerts tumor‐suppressive effects by induction of mesenchymal‐to‐epithelial transition, apoptosis and a less proliferative capacity. Several reports have described miR‐16 as a tumor suppressor microRNA (miRNA). Here, we studied the impact of exogenous induction of miR‐16 in MDA‐MB‐231 and SK‐BR‐3 breast cancer cells following overexpression of miR‐302/367 cluster and investigated whether transfection of these cells by a mature miR‐16 mimic could affect the reprogramming state of the cells and their tumorigenicity. miR‐16 enhanced the expression levels of OCT4A, SOX2, and NANOG, generally known as transcription or pluripotency factors, and suppressed proliferation and invasiveness of these cells. Meanwhile, inhibition of miR‐16 counteracted both the reprogramming effect and the antitumor function of miR‐302/367 in the breast cancer cells. Current results indicate that miR‐16 can work as an adjuvant to improve both cancer cell reprogramming and tumor‐suppressive function of miR‐302/367 cluster in MDA‐MB‐231 and SK‐BR‐3 cells, while its inhibition counteracts all of these effects. Combined application of miRNAs that share some common targets in cancer cell signaling pathways may provide new approaches for repression of multiple hallmarks of cancer.

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Section: Discussionmentioning

confidence: 99%

miR‐16 enhances miR‐302/367‐induced reprogramming and tumor suppression in breast cancer cells

2020

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“…Upregulated miR-31, miR-221, and miR-21 were selected for confirmation from the group of miRNAs specific for HPV-independent tumors including HNC as playing a role in increasing cell proliferation, invasion, and migration [55–58], participating in regulation of epithelial-mesenchymal transition (EMT), or having a prognostic impact [59, 60]. Further choices were miR-34a, specific for HPV-negative tumors, a tumor suppressor whose downregulation has been shown in a number of tumor types including HNC [61, 62], as well as miR-16, the inhibition of which promotes cell proliferation, migration, invasion, and EMT and contributes to tumor progression [63]. The last miRNA selected for confirmation from the group of HPV-negative tumors was miR-193b whose high expression in tissue was identified as an independent prognostic risk factor in patients with ovarian cancer [64].…”

Section: Discussionmentioning

confidence: 99%

Comparison of the miRNA expression profiles in fresh frozen and formalin-fixed paraffin-embedded tonsillar tumors

et al. 2017

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MicroRNAs are considered as promising prognostic and diagnostic biomarkers of human cancer since their profiles differ between tumor types. Most of the tumor profiling studies were performed on rarely available fresh frozen (FF) samples. Alternatively, archived formalin-fixed paraffin-embedded (FFPE) tissue samples are also well applicable to larger-scale retrospective miRNA profiling studies. The aim of this study was to perform systematic comparison of the miRNA expression profiles between FF and macrodissected FFPE tonsillar tumors using the TaqMan Low Density Array system, with the data processed by different software programs and two types of normalization methods. We observed a marked correlation between the miRNA expression profiles of paired FF and FFPE samples; however, only 27-38% of the differentially deregulated miRNAs overlapped between the two source systems. The comparison of the results with regard to the distinct modes of data normalization revealed an overlap in 58–67% of differentially expressed miRNAs, with no influence of the choice of software platform. Our study highlights the fact that for an accurate comparison of the miRNA expression profiles from published studies, it is important to use the same type of clinical material and to test and select the best-performing normalization method for data analysis.

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“…The Snail2 and miR-203 regulatory loop is in concert with miR-200 and ZEB1/2, forming a feed-forward loop to regulate EMT and gene expression [47]. Similarly, the mutual control of miR-145 and ZEB2 contributes to prostate cancer progression and metastasis, wherein ZEB2 directly represses the transcription of miR-145, which in turn represses ZEB2 [48]. These reciprocal feedback loops may explain the reversibility of EMT and MET through an imbalanced expression of miRNAs and EMT transcription factors [49].…”

Section: Micrornas’ Control Of Epithelial-mesenchymal Plasticitymentioning

confidence: 99%

The crosstalk between lncRNA and microRNA in cancer metastasis: orchestrating the epithelial-mesenchymal plasticity

et al. 2016

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Noncoding RNAs (ncRNAs) have been demonstrated to closely associate with gene regulation and encompass the well-known microRNAs (miRNAs), as well as the most recently acknowledged long noncoding RNAs (lncRNAs). Current evidence indicates that lncRNAs can interact with miRNAs and these interactions play crucial roles in cancer metastasis, through regulating critical events especially the epithelial-mesenchymal transition (EMT). This review summarizes the types of lncRNA-miRNA crosstalk identified to-date and discusses their influence on the epithelial-mesenchymal plasticity and clinical metastatic implication.

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MiR-132, miR-15a and miR-16 synergistically inhibit pituitary tumor cell proliferation, invasion and migration by targeting Sox5

Cited by 122 publications

References 24 publications

miR‐16 enhances miR‐302/367‐induced reprogramming and tumor suppression in breast cancer cells

miR‐16 enhances miR‐302/367‐induced reprogramming and tumor suppression in breast cancer cells

Comparison of the miRNA expression profiles in fresh frozen and formalin-fixed paraffin-embedded tonsillar tumors

The crosstalk between lncRNA and microRNA in cancer metastasis: orchestrating the epithelial-mesenchymal plasticity

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