MicroRNA-544 down-regulates both Bcl6 and Stat3 to inhibit tumor growth of human triple negative breast cancer

Zhu, Zhou; Wang, Shengying; Zhu, Junming; Yang, Qifeng; Dong, Hui-Ming; Huang, Jiankang

doi:10.1515/hsz-2016-0104

Cited by 36 publications

(30 citation statements)

References 32 publications

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“…MiR‐544 has been reported to be dysregulated in several cancers. For example, miR‐544 can inhibit human triple negative breast cancer development by inhibiting Bcl6 and STAT3 (Zhu et al, ). miR‐544 is able to restrain the epithelial‐to‐mesenchymal transition (EMT) through targeting the TWIST1 in in carcinoma patients (Haga & Phinney, ).…”

Section: Discussionmentioning

confidence: 99%

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XIST/miR‐544 axis induces neuropathic pain by activating STAT3 in a rat model

Jin¹,

Du²,

Zhao³

et al. 2018

Journal Cellular Physiology

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An increasing number of studies have reported that lncRNAs are responsible for the development of neuropathic pain. In our current study, chronic constriction injury (CCI) rat models were established and we observed that lncRNA XIST was greatly increased. Knockdown of XIST can relieve pain characteristics including both mechanical and thermal hyperalgesia in CCI rats. Meanwhile, XIST down-regulation could inhibit neuro-inflammation by reducing expression of inflammatory cytokines including tumor necrosis factor (TNF)-α, IL-1β, and IL-6 and in CCI rats. By performing bioinformatics technology, miR-544 was predicted to have interactions with XIST and dual-luciferase reporter assays validated the correlation between them. A negative correlation between miR-544 and XIST was observed by carrying out XIST loss or gain of function tests. miR-544 markedly alleviated neuropathic pain development in CCI rats via targeting inflammatory cytokines, which was reversed by XIST over-expression. Moreover, STAT3 was manifested to be a target gene of miR-544 by bioinformatics predictions and it was activated in CCI rats. Over-expression of STAT3 was able to induce neuropathic pain and miR-544 inhibited this process in vivo. Furthermore, XIST increased STAT3 expression by sponging miR-544 in neuropathic pain development. To conclude, our present study indicated that XIST can contribute to neuropathic pain progression in rats through down-regulating miR-544 and up-regulating STAT3. Our results suggested that XIST/miR-544/STAT3 axis can serve as a novel therapeutic target in neuropathic pain development.

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Section: Discussionmentioning

confidence: 99%

“…Error bars stand for the mean ± SD of at least triplicate experiments. *p < 0.05, **p < 0.01 development by inhibiting Bcl6 and STAT3(Zhu et al, 2016). miR-544…”

mentioning

confidence: 97%

XIST/miR‐544 axis induces neuropathic pain by activating STAT3 in a rat model

Jin¹,

Du²,

Zhao³

et al. 2018

Journal Cellular Physiology

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“…Based on the miRNA target predication software, we initially predicted miRNA targets of the top 5 upregulated and validated circRNAs and then subjected them to down-regulated MPE-associated miRNAs， indicating up-regulated circRNAs might inhibit the expression of down-regulated miRNAs. Among the 23 potential miRNAs, some have been reported as important regulaters in many kinds of cancers [42][43][44][45][46][47][48]. For example, L Bao et al revealed that downregulation of miR-298 increased P-Glycoprotein expression and induced doxorubicin resistance in sensitive breast cancer cells, suggesting miR-298 was associated with the chemoresistant mechanisms of metastatic human breast cancer by directly modulating P-Glycoprotein expression [42].…”

Section: Discussionmentioning

confidence: 99%

Microarray expression profile and analysis of circular RNA regulatory network in malignant pleural effusion

et al. 2018

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Malignant pleural effusion (MPE) is a common complication of lung cancer. Accumulating evidence has suggested that circular RNAs (circRNAs) play important roles in oncogenesis and progression of cancer. However, the expression pattern of circRNAs in MPE remains largely unknown and awaits investigation. The study was designed to elucidate the potential roles of differentially expressed circRNAs in MPE. Herein, we detected a total of 1350 differentially expressed circRNAs and 1727 differentially expressed mRNAs in lung adenocarcinoma-associated malignant pleural effusion (LA-MPE) compared with tuberculous pleural effusion (TPE) by Clariom D Human Microarray. Among the top 5 up-regulated circRNAs (hsa_circ_0067705, hsa_circ_0025542, hsa_circ_0072793, hsa_-circ_0084927, and hsa_circ_0085386), four were verified significantly up-regulated in LA-MPE by qRT-PCR and hsa_circ_0085386 had an increasing trend. CircRNA-miRNA-mRNA network for the top 5 upregulated circRNAs was constructed and pathway analysis indicated that the enriched mRNA targets involved in PI3K-Akt signaling pathway, Axon guidance, Regulation of actin cytoskeleton and Rap1 signaling pathway were potentially regulated by these aberrantly expressed circRNAs. We generated specific circRNA profiles in LA-MPE for the first time. And analysis of circRNA regulatory network could provide evidence that circRNAs are important in MPE development because they participate in cancer-related pathways by sequestering miRNAs. Our findings suggested that aberrantly expressed circRNAs may be involved in the development of LA-MPE. ARTICLE HISTORY

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“…However, IL-6 or HIF-1A-induce STAT3 and InH3 expression, resulting in the induction of invasion and metastasis of CRC by repression of miR-34a [205]. Moreover, miR-216 inhibits the activation of JAK2/STAT3 signaling by reducing JAK2 expression [206], and miR-544 suppresses the expression of both Bcl6 and STAT3 by direct targeting [207]. Furthermore, miR-26a inhibits metastasis through the downregulation of IL-6 expression by reducing the expression of Lin-28 homolog B (LIN28B), HMGA1, and MITF as a direct target and through the restoration of LIN28B-reduced let7d expression [208,209].…”

Section: Micrornas As Negative Regulatorsmentioning

confidence: 99%

Role of JAK/STAT3 Signaling in the Regulation of Metastasis, the Transition of Cancer Stem Cells, and Chemoresistance of Cancer by Epithelial–Mesenchymal Transition

Jin

2020

Cells

316

193

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The JAK/STAT3 signaling pathway plays an essential role in various types of cancers. Activation of this pathway leads to increased tumorigenic and metastatic ability, the transition of cancer stem cells (CSCs), and chemoresistance in cancer via enhancing the epithelial–mesenchymal transition (EMT). EMT acts as a critical regulator in the progression of cancer and is involved in regulating invasion, spread, and survival. Furthermore, accumulating evidence indicates the failure of conventional therapies due to the acquisition of CSC properties. In this review, we summarize the effects of JAK/STAT3 activation on EMT and the generation of CSCs. Moreover, we discuss cutting-edge data on the link between EMT and CSCs in the tumor microenvironment that involves a previously unknown function of miRNAs, and also discuss new regulators of the JAK/STAT3 signaling pathway.

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MicroRNA-544 down-regulates both Bcl6 and Stat3 to inhibit tumor growth of human triple negative breast cancer

Cited by 36 publications

References 32 publications

XIST/miR‐544 axis induces neuropathic pain by activating STAT3 in a rat model

XIST/miR‐544 axis induces neuropathic pain by activating STAT3 in a rat model

Microarray expression profile and analysis of circular RNA regulatory network in malignant pleural effusion

Role of JAK/STAT3 Signaling in the Regulation of Metastasis, the Transition of Cancer Stem Cells, and Chemoresistance of Cancer by Epithelial–Mesenchymal Transition

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