Regulation of STAT3 by miR-106a is linked to cognitive impairment in ovariectomized mice

Zhang, Min; Ye, Yuqin; Cong, Jing; Pu, Danhua; Liu, Jiayin; Hu, Gang; Wu, Jie

doi:10.1016/j.brainres.2013.01.052

Cited by 21 publications

(15 citation statements)

References 57 publications

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“…In our in silico model, luciferase reporter assays and in vitro functional analyses, we demonstrated that miR‐106a, miR‐18b and miR‐363‐3p can bind to the 3′ UTR of Nfat5 and Rora , leading to a consequent decrease of Il17a/f gene expression and reduction of Il‐17a protein production. This might be further amplified by additional binding of these miRNAs to the transcription factor Stat3 , as has been shown for miR‐106a . Stat3 is, next to Ror α and Ror γ t, essential for Th17 differentiation and Il17 gene expression .…”

Section: Discussionmentioning

confidence: 93%

microRNA cluster 106a~363 is involved in T helper 17 cell differentiation

Kästle

Bartel²,

Geillinger-Kästle³

et al. 2017

Immunology

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T-helper cell type 17 (Th17) mediated inflammation is associated with various diseases including autoimmune encephalitis, inflammatory bowel disease and lung diseases such as chronic obstructive pulmonary disease and asthma. Differentiation into distinct T helper subtypes needs to be tightly regulated to ensure an immunological balance. As microRNAs (miRNAs) are critical regulators of signalling pathways, we aimed to identify specific miRNAs implicated in controlling Th17 differentiation. We were able to create a regulatory network model of murine T helper cell differentiation by combining Affymetrix mRNA and miRNA arrays and in silico analysis. In this model, the miR-212~132 and miR-182~183 clusters were significantly up-regulated upon Th17 differentiation, whereas the entire miR-106~363 cluster was down-regulated and predicted to target well-known Th17 cell differentiation pathways. In vitro transfection of miR-18b, miR-106a and miR-363-3p into primary murine Cd4 lymphocytes decreased expression of retinoid-related orphan receptor c (Rorc), Rora, Il17a and Il17f, and abolished secretion of Th17-mediated interleukin-17a (Il17a). Moreover, we demonstrated target site-specific regulation of the Th17 transcription factors Rora and nuclear factor of activated T cells (Nfat) 5 by miR-18b, miR-106a and miR-363-3p through luciferase reporter assays. Here, we provide evidence that miRNAs are involved in controlling the differentiation and function of T helper cells, offering useful tools to study and modify Th17-mediated inflammation.

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Section: Discussionmentioning

confidence: 93%

microRNA cluster 106a~363 is involved in T helper 17 cell differentiation

Kästle

Bartel²,

Geillinger-Kästle³

et al. 2017

Immunology

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show abstract

“…16 Interestingly, our recent study showed that miR-106a regulation of signal transducer and activator of transcription 3 (STAT3) expression was linked to cognitive impairment in ovariectomized mice. 17 MiR-106a, a member of the miR-17-92 cluster sharing the same AAAGUGC seedYcontaining sequence, is abundantly expressed in the hippocampus. 18,19 Podolska et al 20 reported that miR-106a, which was highly expressed in porcine fetal tissue, might be involved in the development and growth of a particular region of the brain such as the frontal cortex or cerebellum.…”

mentioning

confidence: 99%

Expression of early growth response 1 affects miR-106a/signal transducer and activator of transcription 3 regulating cognitive impairment in ovariectomized mice

Cong

Wang

Pu³

et al. 2014

Menopause

Self Cite

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“…To explore the role of miRNAs in STAT3-HIF-1α, we used TargetScan to predict the target gene of them. We find that both STAT3 and HIF-1α might be regulated by commen miRNAs such as miR-1724, miR-20a24, miR-20b25, miR-106a26, miR-106b27, miR-1724 and miR-9328, which were previously verified as the target genes of STAT3, and miR-20a29, miR-20b30, miR-1731 and miR-9332 were previously verified as the target genes of HIF-1α. Interestingly, we found that EMMPRIN suppressed miR-106a and miR-106b expression in breast cancer cells significantly.…”

Section: Discussionmentioning

confidence: 64%

EMMPRIN Down-regulating miR-106a/b Modifies Breast Cancer Stem-like Cell Properties via Interaction with Fibroblasts Through STAT3 and HIF-1α

Liu

Zhang

Sun

et al. 2016

Sci Rep

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Extracellular matrix metalloproteinase inducer (EMMPRIN) is a heavily glycosylated protein and expresses in cancer cells widely, which plays important roles in tumor progression. However, the role of EMMPRIN in breast cancer stem-like cell properties by interaction with fibroblasts is not known. In the present study, we investigated the effects of fibroblasts on breast cancer stem-like cells. We found that fibroblasts activated by co-cultured breast cancer cells produced higher levels of EMMPRIN, which stimulated the stem-like cell specific, self-renewal and sphere-forming phenotype in breast cancer cells. Increased EMMPRIN expression in activated fibroblasts increased the expression of STAT3 and HIF-1α and showed cancer stem-like cell features in breast cancer cells. We also found that EMMPRIN could down-regulate miR-106a and miR-106b expression in breast cancer cells, which led to activating STAT3 and enhancing HIF-1α expression. Our results illustrated that EMMPRIN has an important role in breast cancer stem-like cells by activation STAT3/HIF-1α through interaction with cancer cells and fibroblasts. The study for the first time indicated that cancer cells and fibroblasts interaction promotes breast cancer cells showing stem-like cells through up-regulation EMMPRIN, and led to inhibiting miR-106a/b expression which targets both STAT3 and HIF-1α expression.

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Regulation of STAT3 by miR-106a is linked to cognitive impairment in ovariectomized mice

Cited by 21 publications

References 57 publications

microRNA cluster 106a~363 is involved in T helper 17 cell differentiation

microRNA cluster 106a~363 is involved in T helper 17 cell differentiation

Expression of early growth response 1 affects miR-106a/signal transducer and activator of transcription 3 regulating cognitive impairment in ovariectomized mice

EMMPRIN Down-regulating miR-106a/b Modifies Breast Cancer Stem-like Cell Properties via Interaction with Fibroblasts Through STAT3 and HIF-1α

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