Regulation rewiring analysis reveals mutual regulation between STAT1 and miR-155-5p in tumor immunosurveillance in seven major cancers

Chen, Lin; Jiang, Wei; Mitra, Ramkrishna; Cheng, Feixiong; Yu, Hui; Zhao, Zhongming

doi:10.1038/srep12063

Cited by 20 publications

(21 citation statements)

References 65 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As another important TF involved in carcinogenesis, STAT1 has been reported to interact with miR-155 [24]. In the present study, we confirmed the inhibitory function of miR-155 on STAT1, which leads to miR-155-induced CRC growth.…”

Section: Discussionsupporting

confidence: 87%

The miR-124-p63 feedback loop modulates colorectal cancer growth

et al. 2017

View full text Add to dashboard Cite

Among the diverse co-regulatory relationships between transcription factors (TFs) and microRNAs (miRNAs), feedback loops have received the most extensive research attention. The co-regulation of TFs and miRNAs plays an important role in colorectal cancer (CRC) growth. Here, we show that miR-124 can regulate two isoforms of p63, TAp63 and ΔNp63, via iASPP, while p63 modulates signal transducers and activators of transcription 1 (STAT1) expression by targeting miR-155. Moreover, STAT1 acts as a regulator of CRC growth by targeting miR-124. Taken together, these results reveal a feedback loop between miRNAs and TFs. This feedback loop comprises miR-124, iASPP, STAT1, miR-155, TAp63 and ΔNp63, which are essential for CRC growth. Moreover, this feedback loop is perturbed in human colon carcinomas, which suggests that the manipulation of this microRNA-TF feedback loop has therapeutic potential for CRC.

show abstract

Section: Discussionsupporting

confidence: 87%

The miR-124-p63 feedback loop modulates colorectal cancer growth

et al. 2017

View full text Add to dashboard Cite

show abstract

“… 2014 ; Lin et al. 2015 ). Interestingly, when measuring STAT-1 and MAP kinase, we found that the phosphorylation of STAT-1 and ERK, P-38, JNK was reduced in congruence with increased concentrations of curcumin ( Figure 5(A) ).…”

Section: Resultsmentioning

confidence: 99%

Anti-inflammatory effects of curcumin are associated with down regulating microRNA-155 in LPS-treated macrophages and mice

Liu

Ding

et al. 2017

Pharmaceutical Biology

103

View full text Add to dashboard Cite

Context: The natural polyphenolic compound curcumin has been proved to modulate innate immune responses and possess anti-inflammatory properties. Nevertheless, the mechanism remains poorly understood, particularly regarding curcumin-regulated miRNAs under inflammatory response.Objective: This study investigates the role of miRNA-155 in the effects of curcumin on inflammatory response in cell and a mouse model.Materials and methods: The anti-inflammatory activity of curcumin (5, 10 and 15 μM, 2 h) in lipopolysaccharide (LPS, 200 ng/mL)-induced cells were measured by quantitative PCR. The animals were treated orally by 20 mg/kg curcumin for 3 days before an LPS intraperitoneal injection (10 mg/kg, 16 h). MicroRNA (miRNA) expression and the underlying molecular mechanisms were assessed using transfection technique and western blotting.Results and discussion: Curcumin efficiently inhibited LPS-induced cytokines (TNF-α, IL-6) and microRNA-155 (miR-155) expression (p < 0.05) without affecting the normally growth of Raw264.7 and THP-1 cells (IC50 21.8 and 22.3 μM at 48 h, respectively). Moreover, the levels of cytokines were suppressed by curcumin in miR-155 mimics transfected cells (p < 0.05). A blockade of PI3K/AKT signalling pathways resulted in a decreased level of miR-155 (p < 0.05). Curcumin effectively protected mice from sepsis as evidenced by decreasing histological damage, reducing AST (352.0 vs 279.3 U/L), BUN (14.8 vs 10.8 mmol/L) levels and the proportion of macrophages in spleen (31.1% vs 13.5%). MicroRNA-155 level and cytokines were also reduced in curcumin-treated mice (p < 0.05).Conclusions: Curcumin’s ability to suppress LPS-induced inflammatory response may be due to the inhibition of miR-155.

show abstract

“…A bioinformatic study conducted across seven cancer types found that gene modules representing MHC class I function are highly expressed, and that within these modules, the most up-regulated proteasome subunits are PSMB8 and PSMB9 43. Here, the expression of IP subunit PSMB8 correlated with RARRES3 in BM-MSC and four tumor datasets, and also correlated with HLA-C in all but one of these cancer types.…”

Section: Discussionmentioning

confidence: 72%

The metastasis suppressor RARRES3 as an endogenous inhibitor of the immunoproteasome expression in breast cancer cells

Anderson

Kalimutho

Harten

et al. 2017

Sci Rep

View full text Add to dashboard Cite

In breast cancer metastasis, the dynamic continuum involving pro-and anti-inflammatory regulators can become compromised. Over 600 genes have been implicated in metastasis to bone, lung or brain but how these genes might contribute to perturbation of immune function is poorly understood. To gain insight, we adopted a gene co-expression network approach that draws on the functional parallels between naturally occurring bone marrow-derived mesenchymal stem cells (BM-MSCs) and cancer stem cells (CSCs). Our network analyses indicate a key role for metastasis suppressor RARRES3, including potential to regulate the immunoproteasome (IP), a specialized proteasome induced under inflammatory conditions. Knockdown of RARRES3 in near-normal mammary epithelial and breast cancer cell lines increases overall transcript and protein levels of the IP subunits, but not of their constitutively expressed counterparts. RARRES3 mRNA expression is controlled by interferon regulatory factor IRF1, an inducer of the IP, and is sensitive to depletion of the retinoid-related receptor RORA that regulates various physiological processes including immunity through modulation of gene expression. Collectively, these findings identify a novel regulatory role for RARRES3 as an endogenous inhibitor of IP expression, and contribute to our evolving understanding of potential pathways underlying breast cancer driven immune modulation.

show abstract

Regulation rewiring analysis reveals mutual regulation between STAT1 and miR-155-5p in tumor immunosurveillance in seven major cancers

Cited by 20 publications

References 65 publications

The miR-124-p63 feedback loop modulates colorectal cancer growth

The miR-124-p63 feedback loop modulates colorectal cancer growth

Anti-inflammatory effects of curcumin are associated with down regulating microRNA-155 in LPS-treated macrophages and mice

The metastasis suppressor RARRES3 as an endogenous inhibitor of the immunoproteasome expression in breast cancer cells

Contact Info

Product

Resources

About