FOXP3 and miR-155 cooperate to control the invasive potential of human breast cancer cells by down regulating ZEB2 independently of ZEB1

Brown, Cheryl Y.; Dayan, Sonia; Wong, Soon Wei; Kaczmarek, Adrian; Hope, Christopher; Pederson, Stephen; Arnet, Victoria; Goodall, Gregory J.; Russell, Darryl L.; Sadlon, Timothy; Barry, Simon C.

doi:10.18632/oncotarget.25523

Cited by 21 publications

(16 citation statements)

References 63 publications

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“…MiR-155 plays crucial roles in the immune response, tumorigenesis and stem cell differentiation [33][34][35][36] and has been reported to target and repress many genes including SOCS1, TNF-α, and SHIP1 [18][19][20]. Dudda et al reported that miR-155 and its target gene, SOCS1, are key regulators of effector CD8( +) T cells as they affect cytokine signaling through STAT5 [37].…”

Section: Discussionmentioning

confidence: 99%

Luteolin inhibits respiratory syncytial virus replication by regulating the MiR-155/SOCS1/STAT1 signaling pathway

Wang

Ling

Yao

et al. 2020

Virol J

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Background Respiratory syncytial virus (RSV) is a major cause of acute lower respiratory tract infection in infants, children, immunocompromised adults, and elderly individuals. Currently, there are few therapeutic options available to prevent RSV infection. The present study aimed to investigate the effects of luteolin on RSV replication and the related mechanisms. Material and methods We pretreated cells and mice with luteolin before infection with RSV, the virus titer, expressions of RSV-F, interferon (IFN)-stimulated genes (ISGs), and production of IFN-α and IFN-β were determined by plaque assay, RT-qPCR, and ELISA, respectively. The activation of Janus kinase (JAK)-signal transducer and activator of transcription 1 (STAT1) signaling pathway was detected by Western blotting and luciferase assay. Proteins which negatively regulate STAT1 were determined by Western blotting. Then cells were transfected with suppressor of cytokine signaling 1 (SOCS1) plasmid and virus replication and ISGs expression were determined. Luciferase reporter assay and Western blotting were performed to detect the relationship between SOCS1 and miR-155. Results Luteolin inhibited RSV replication, as shown by the decreased viral titer and RSV-F mRNA expression both in vitro and in vivo. The antiviral activity of luteolin was attributed to the enhanced phosphorylation of STAT1, resulting in the increased production of ISGs. Further study showed that SOCS1 was downregulated by luteolin and SOCS1 is a direct target of microRNA-155 (miR-155). Inhibition of miR-155 rescued luteolin-mediated SOCS1 downregulation, whereas upregulation of miR-155 enhanced the inhibitory effect of luteolin. Conclusion Luteolin inhibits RSV replication by regulating the miR-155/SOCS1/STAT1 signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Luteolin inhibits respiratory syncytial virus replication by regulating the MiR-155/SOCS1/STAT1 signaling pathway

Wang

Ling

Yao

et al. 2020

Virol J

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“…Moreover, ZEB2 plays a synergistic effect with cdc42 GTPase-activating protein, as a novel E-cadherin transcriptional repressor, to facilitate breast cancer tumor growth and metastasis to lung [40]. Previous studies also uncover that ZEB2 can be regulated by miRNAs, including miR-29b, miR-30a, miR-155, miR-204 and miR-205, in the development of breast cancer aggressiveness [26,27,39,41,42]. In the present study, our findings extended the role of ZEB2, as an oncogene promotion of cell proliferation in breast cancer, that was a direct target of miR-653.…”

Section: Discussionmentioning

confidence: 99%

“…Numerous studies also reveal that ZEB2 contributes to breast cancer progression by coordinating EMT [24,25]. Post-transcriptional regulatory mechanism has been shown that miR-30a, miR-155 and miR-200 family members inhibit human breast cancer cells invasion by down-regulating ZEB2 [26,27]. However, the association between circRNA and ZEB2 in the pathogenesis of breast cancer is still unclear.…”

Section: Introductionmentioning

confidence: 99%

Silencing of hsa_circ_0004771 inhibits proliferation and induces apoptosis in breast cancer through activation of miR-653 by targeting ZEB2 signaling pathway

et al. 2019

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Background: Circular RNAs (circRNAs) have been reported as the competing endogenous RNAs (ceRNAs) to sponge microRNAs (miRNAs) implicating in the initiation and progression of breast cancer. However, the functions of circRNAs in breast cancer have not been completely clarified. In the present study, we aimed to identify differentially expressed circRNAs in breast cancer tumor tissues, and their roles and downstream targets were investigated in the progression of breast cancer. Methods: High-throughput circRNA sequencing was performed to detect the differentially expressed circRNAs. The CCK-8 and flow cytometry were performed to measure the cell viability and apoptosis in breast cancer cells. Gene and protein expression were assayed by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and Western blotting, respectively. Results: hsa_circ_0004771 and Zinc finger E-box binding homeobox 2 (ZEB2) expression levels were up-regulated and positively correlated in breast cancer tumor tissues. In addition, the expression levels of miR-653 were reduced in breast cancer tumor tissues. We also found that hsa_circ_0004771 functioned as a sponge of miR-653 to inhibit its expression. miR-653 as a post-transcriptional regulator down-regulated the expression of ZEB2 by binding to its 3′-UTR. Interestingly, a significant inverse correlation was observed between miR-653 and hsa_circ_0004771 or ZEB2 expression in breast cancer tumor tissues. Knockdown of hsa_circ_0004771 and ZEB2 served as equally authentic of miR-653 mimics to induce growth inhibition and apoptosis in breast cancer cells. Conclusion: Hsa_circ_0004771/miR-653/ZEB2 regulatory feedback revealed a new molecular mechanism in the pathogenesis of breast cancer, which might provide novel therapeutic targets for the treatment of breast cancer.

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“…SATB1 interactions with transcription activators and repressors are determined by its post-transcriptional modifications like phosphorylation or acetylation [22,23]. It was shown that STAB1 can also be regulated by numerous microRNAs, including miR-191, miR-155, miR-448, miR-7, miR-302a-3p and miR-21-5p [24,25,26,27,28,29,30]. SATB1 regulates gene expression on a tissue-specific manner—it binds to distinct genomic regions and regulates different sets of genes depending on the cell type [31].…”

Section: Introductionmentioning

confidence: 99%

The Role of SATB1 in Tumour Progression and Metastasis

Glatzel-Plucińska

Piotrowska

Dzięgiel

et al. 2019

IJMS

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Carcinogenesis is a long-drawn, multistep process, in which metastatic spread is an unequivocal hallmark of a poor prognosis. The progression and dissemination of epithelial cancers is commonly thought to rely on the epidermal-mesenchymal transition (EMT) process. During EMT, epithelial cells lose their junctions and apical-basal polarity, and they acquire a mesenchymal phenotype with its migratory and invasive capabilities. One of the proteins involved in cancer progression and EMT may be SATB1 (Special AT-Rich Binding Protein 1)—a chromatin organiser and a global transcriptional regulator. SATB1 organizes chromatin into spatial loops, providing a “docking site” necessary for the binding of further transcription factors and chromatin modifying enzymes. SATB1 has the ability to regulate whole sets of genes, even those located on distant chromosomes. SATB1 was found to be overexpressed in numerous malignancies, including lymphomas, breast, colorectal, prostate, liver, bladder and ovarian cancers. In the solid tumours, an elevated SATB1 level was observed to be associated with an aggressive phenotype, presence of lymph node, distant metastases, and a poor prognosis. In this review, we briefly describe the prognostic significance of SATB1 expression in most common human cancers, and analyse its impact on EMT and metastasis.

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FOXP3 and miR-155 cooperate to control the invasive potential of human breast cancer cells by down regulating ZEB2 independently of ZEB1

Cited by 21 publications

References 63 publications

Luteolin inhibits respiratory syncytial virus replication by regulating the MiR-155/SOCS1/STAT1 signaling pathway

Luteolin inhibits respiratory syncytial virus replication by regulating the MiR-155/SOCS1/STAT1 signaling pathway

Silencing of hsa_circ_0004771 inhibits proliferation and induces apoptosis in breast cancer through activation of miR-653 by targeting ZEB2 signaling pathway

The Role of SATB1 in Tumour Progression and Metastasis

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