lncRNA XIST interacts with miR-140 to modulate lung cancer growth by targeting iASPP

Tang, Yongjun; He, Ruoxi; An, Jian; Deng, Pengbo; Huang, Li; Yang, Wei

doi:10.3892/or.2017.5751

Cited by 51 publications

(43 citation statements)

References 39 publications

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“…Interestingly, numerous research reported that as an oncogenic lncRNA, XIST promoted tumor proliferation and inhibited tumor apoptosis. Tang et al (2017) suggested that XIST promoted the proliferation and metastasis of lung cancer.…”

Section: Discussionmentioning

confidence: 99%

LncRNA XIST regulates myocardial infarction by targeting miR‐130a‐3p

Zhou

Qin

Yang

et al. 2018

Journal Cellular Physiology

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The study was employed to probe long non-coding RNA X-inactive specific transcript RNA (lncRNA XIST) expression profile and its influence on cell cycle, proliferation and apoptosis in myocardial cells. We also aimed to explore the possible meditating relationship between XIST, PDE4D and miR-130a-3p. Gene differential analysis was carried out using Human LncRNA Microarray V3.0. Quantitative real-time PCR (qRT-PCR) was used to test mRNA expressions of XIST, miR-130a-3p and PDE4D in normal cells and post-myocardial infarction (MI) cells. Western blot was applied to determine the protein expression profile of PED4D. Changes in viability and cell cycle/apoptosis of post-MI myocardial cells after silencing of XIST or PDE4D were investigated by MTT assay and flow cytometry, respectively. The targeting relationship between miR-130a-3p and XIST, PDE4D in myocardial cells were verified by dual luciferase reporter assay. Simulated MI environment was constructed by performing anoxic preconditioning in normal cells to probe the influence of XIST on myocardial cell apoptosis. XIST and PDE4D were overexpressed in post-MI myocardial cells, while miR-130a-3p was underexpressed in post-MI myocardial cells. High-expressed XIST and PDE4D both promoted myocardial cell apoptosis. High-expressed XIST also inhibited myocardial cell proliferation. XIST down-regulated miR-130a-3p and PDE4D was a direct target of miR-130a-3p. LncRNA XIST promotes MI by targeting miR-130a-3p. MI induced by PDE4D can be reversed by miR-130a-3p. This article is protected by copyright. All rights reserved.

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Section: Discussionmentioning

confidence: 99%

LncRNA XIST regulates myocardial infarction by targeting miR‐130a‐3p

Zhou

Qin

Yang

et al. 2018

Journal Cellular Physiology

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“…XIST can promote esophageal squamous cell carcinoma via regulating miR‐101/EZH2 axis (Wu et al, ). It is reported that XIST serve as an oncogenic lncRNA, which can promote the proliferation and metastasis of lung cancer via sponging miR‐140 (Tang et al, ). XIST can lead to neuronal apoptosis by inhibiting AKT phosphorylation and it is down‐regulated by miR‐494 in rat spinal cord injury (Gu et al, ).…”

Section: Discussionmentioning

confidence: 99%

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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“…Since a lot of classic signal pathways that are regulated by miRNAs, such as JNK [83], Wnt/β-catenin signaling pathway [84], or MAPK [85], also influence the expression of several lncRNAs in lung cancer tissues, it is safe to presume that some of the classic tumor-associated pathways are coregulated by lncRNAs and miRNAs. For example, miR-21 influences GAS5′s regulation of NSCLC cisplatin sensitivity through the PTEN pathway [86], and lncRNA-XIST can promote proliferation and metastases in lung cancer via miR-140 regulation of the p53 (inhibitor of apoptosis-stimulating protein of p53-iASPP) pathway [87].…”

Section: Long Noncoding Rnasmentioning

confidence: 99%

“…New target therapies, such as EGFR-activating tyrosine kinase inhibitors (TKI), confirmed their superiority to chemotherapy and research focused especially on EGFR-activating mutations and abnormal gene fusion between echinoderm microtubule-associated protein-like 4 and anaplastic lymphoma kinase (EML4-ALK) [24,25,[87][88][89]. In order to detect the presence of mutations, repeated invasive examinations are required, which can cause discomfort to the patient.…”

Section: Liquid Biopsy In Lung Cancermentioning

confidence: 99%

Noncoding RNAs and Liquid Biopsy in Lung Cancer: A Literature Review

et al. 2019

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Lung cancer represents a genetically heterogeneous disease with low survival rates. Recent data have evidenced key roles of noncoding RNAs in lung cancer initiation and progression. These functional RNA molecules that can act as both oncogenes and tumor suppressors may become future biomarkers and more efficient therapeutic targets. In the precision medicine era, circulating nucleic acids have the potential to reshape the management and prognosis of cancer patients. Detecting genomic alterations and level variations of circulating nucleic acids in liquid biopsy samples represents a noninvasive method for portraying tumor burden. Research is currently trying to validate the potential role of liquid biopsy in lung cancer screening, prognosis, monitoring of disease progression, and treatment response. However, this method requires complex detection assays, and implementation of plasma genotyping in clinical practice continues to be hindered by discrepancies that arise when compared to tissue genotyping. Understanding the genomic landscape of lung cancer is essential in order to provide useful and innovative research in the age of patient-tailored therapy. In this landscape, the noncoding RNAs play a crucial role due to their target genes that dramatically influence the tumor microenvironment and the response to therapy. This article addresses present and future possible roles of liquid biopsy in lung cancer. It also discusses how the complex role of noncoding RNAs in lung tumorigenesis could influence the management of this pathology.

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lncRNA XIST interacts with miR-140 to modulate lung cancer growth by targeting iASPP

Cited by 51 publications

References 39 publications

LncRNA XIST regulates myocardial infarction by targeting miR‐130a‐3p

LncRNA XIST regulates myocardial infarction by targeting miR‐130a‐3p

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

Noncoding RNAs and Liquid Biopsy in Lung Cancer: A Literature Review

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