MicroRNA-155 broadly orchestrates inflammation-induced changes of microRNA expression in breast cancer

Hu, Song; Zhu, Wei; Zhang, Ling-Fei; Pei, Ming; Lin, Li

doi:10.1038/cr.2013.137

Cited by 19 publications

(10 citation statements)

References 9 publications

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“…To this end, we first searched for potential transcription factor-binding sites in MIR489 promoter using the PROMO and TransFac programs (24,25). Interestingly, ETS1 and YY1, 2 transcription factors that have been shown to control miRNA expression in cancer cells (26,27), were predicted as candidate transcription factors for MIR489 ( Fig. 2A, top).…”

Section: Mir-489 Is Downregulated By the Kras/nf-kb/yy1 Axis In Pdac mentioning

confidence: 99%

KRAS/NF-κB/YY1/miR-489 Signaling Axis Controls Pancreatic Cancer Metastasis

Yuan

Rong

et al. 2017

Cancer Research

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KRAS activation occurring in more than 90% of pancreatic ductal adenocarcinomas (PDAC) drives progression and metastasis, but the underlying mechanisms involved in these processes are still poorly understood. Here, we show how KRAS acts through inflammatory NF-κB signaling to activate the transcription factor YY1, which represses expression of the tumor suppressor gene miR-489. In PDAC cells, repression of miR-489 by KRAS signaling inhibited migration and metastasis by targeting the extracellular matrix factors ADAM9 and MMP7. miR-489 downregulation elevated levels of ADAM9 and MMP7, thereby enhancing the migration and metastasis of PDAC cells. Together, our results establish a pivotal mechanism of PDAC metastasis and suggest miR-489 as a candidate therapeutic target for their attack. Cancer Res; 77(1); 100-11. ©2016 AACR.

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Section: Mir-489 Is Downregulated By the Kras/nf-kb/yy1 Axis In Pdac mentioning

confidence: 99%

KRAS/NF-κB/YY1/miR-489 Signaling Axis Controls Pancreatic Cancer Metastasis

Yuan

Rong

et al. 2017

Cancer Research

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“…During the preparation of this manuscript, miR-149 was also found to be downregulated in osteoarthritis chondrocytes and it is correlated with increased expression of inflammatory cytokines including IL-6 59 . Moreover, IL-6 is an important regulator of miRNA expression 60 . Therefore, IL-6 might be a pivot of miR-mediated inflammation in tumor microenvironment.…”

Section: Discussionmentioning

confidence: 99%

Epigenetic silencing of microRNA-149 in cancer-associated fibroblasts mediates prostaglandin E2/interleukin-6 signaling in the tumor microenvironment

et al. 2015

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Tumor initiation and growth depend on its microenvironment in which cancer-associated fibroblasts (CAFs) in tumor stroma play an important role. Prostaglandin E2 (PGE2) and interleukin (IL)-6 signal pathways are involved in the crosstalk between tumor and stromal cells. However, how PGE2-mediated signaling modulates this crosstalk remains unclear. Here, we show that microRNA (miR)-149 links PGE2 and IL-6 signaling in mediating the crosstalk between tumor cells and CAFs in gastric cancer (GC). miR-149 inhibited fibroblast activation by targeting IL-6 and miR-149 expression was substantially suppressed in the CAFs of GC. miR-149 negatively regulated CAFs and their effect on GC development both in vitro and in vivo. CAFs enhanced epithelial-to-mesenchymal transition (EMT) and the stem-like properties of GC cells in a miR-149-IL-6-dependent manner. In addition to IL-6, PGE2 receptor 2 (PTGER2/EP2) was revealed as another potential target of miR-149 in fibroblasts. Furthermore, H. pylori infection, a leading cause of human GC, was able to induce cyclooxygenase-2 (COX-2)/PGE2 signaling and to enhance PGE2 production, resulting in the hypermethylation of miR-149 in CAFs and increased IL-6 secretion. Our findings indicate that miR-149 mediates the crosstalk between tumor cells and CAFs in GC and highlight the potential of interfering miRNAs in stromal cells to improve cancer therapy.

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“…miRNAs are involved in diverse physiological and pathological processes and environmental stresses, including cell proliferation [ 1 ], differentiation [ 1 ], apoptosis [ 2 ], autophagy [ 3 ], tumorigenesis [ 4 ], and even epigenetic regulation [ 5 ]. The expression of miRNAs is regulated by many factors associated with various environmental stresses, such as starvation [ 6 ], nutrition shortage [ 7 ], hypoxia, inflammation [ 8 ], oxidative stimulation, and even anti-cancer drug treatments. Emerging studies have reported that miRNA expression is altered under these stresses through crosstalk with the tumor microenvironment.…”

Section: Introductionmentioning

confidence: 99%

CREB1-driven expression of miR-320a promotes mitophagy by down-regulating VDAC1 expression during serum starvation in cervical cancer cells

Zhang

Wan

et al. 2015

Oncotarget

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The altered expression of miRNAs in response to stresses contributes to cancer pathogenesis. However, little is known regarding the mechanism by which cellular stresses drive alterations in miRNA expression. Here, we found that serum starvation enhanced mitophagy by downregulating the mitophagy-associated protein voltage-dependent anion channel 1 (VDAC1) and by inducing the expression of miR-320a and the transcription factor cAMP responsive element binding protein 1(CREB1). Furthermore, we cloned the promoter of miR-320a and identified the core promoter of miR-320a in the upstream −16 to −130 region of pre-miR-320a. Moreover, CREB1 was found to bind to the promoter of miR-320a to activate its expression and to induce mitophagy during serum starvation. Collectively, our results reveal a new mechanism underlying serum starvation-induced mitophagy in which serum starvation induces CREB1 expression, in turn activating miR-320a expression, which then down-regulates VDAC1 expression to facilitate mitophagy. These findings may provide new insights into cancer cell survival in response to environmental stresses.

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MicroRNA-155 broadly orchestrates inflammation-induced changes of microRNA expression in breast cancer

Cited by 19 publications

References 9 publications

KRAS/NF-κB/YY1/miR-489 Signaling Axis Controls Pancreatic Cancer Metastasis

KRAS/NF-κB/YY1/miR-489 Signaling Axis Controls Pancreatic Cancer Metastasis

Epigenetic silencing of microRNA-149 in cancer-associated fibroblasts mediates prostaglandin E2/interleukin-6 signaling in the tumor microenvironment

CREB1-driven expression of miR-320a promotes mitophagy by down-regulating VDAC1 expression during serum starvation in cervical cancer cells

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