Knockdown of long non-coding RNA XIST exerts tumor-suppressive functions in human glioblastoma stem cells by up-regulating miR-152

Yao, Yilong; Ma, Jun; Xue, Yixue; Wang, Ping; Li, Zhen; Liu, Jing; Chen, Liang‐Yu; Xi, Zhuo; Teng, Hao Wei; Wang, Zhenhua; Li, Zhiqing; Liu, Yunhui

doi:10.1016/j.canlet.2014.12.051

Cited by 323 publications

(273 citation statements)

References 45 publications

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“…Therefore, knockdown of XIST was performed in our study to explore the biological function of XIST. A previous study showed that XIST downregulation exerts tumorsuppressive functions by reducing cell proliferation, migration, and invasion as well as inducing apoptosis in GSCs [17] . While XIST has been reported to be a potent suppressor of hematological cancer [26] , our results revealed that knockdown of XIST promotes NSCLC cell apoptosis and inhibits cell proliferation, migration and invasion.…”

Section: Discussionmentioning

confidence: 96%

“…Moreover, XIST has been found to be dysregulated in a variety of human cancers, and this dysfunctional expression has been shown to exert a pathological role [16] . Recent studies have suggested that the expression of XIST is associated with glioma stem cells (GSCs) in human glioma [17] . However, the function of XIST in lung cancer, particularly in NSCLC, remains a mystery.…”

Section: Acta Pharmacologica Sinicamentioning

confidence: 99%

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The lncRNA XIST exhibits oncogenic properties via regulation of miR-449a and Bcl-2 in human non-small cell lung cancer

Zhang

Hou

et al. 2017

Acta Pharmacol Sin

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Long non-coding RNAs (lncRNAs) are associated with the occurrence, development and prognoses of non-small cell lung cancer (NSCLC). In the present study, we investigated the functional mechanisms of the lncRNA XIST in two human NSCLC cell lines, A549 and NCI-H1299. In all the 5 NSCLC cell lines (NL9980, NCI-H1299, NCI-H460, SPC-A-1 and A549) tested, the expression levels of XIST were significantly elevated, as compared with those in normal human bronchial epithelial cell line BEAS-2B. In A549 and NCI-H1299 cells, knockdown of XIST by siRNA significantly inhibited the cell proliferation, migration and invasion, and promoted cell apoptosis. Furthermore, XIST knockdown elevated the expression of E-cadherin, and suppressed the expression of Bcl-2. Moreover, knockdown of XIST significantly suppressed the tumor growth in NSCLC A549 xenograft mouse model. Bioinformatic analysis and luciferase reporter assays revealed that XIST was negatively regulated by miR-449a. We further identified reciprocal repression between XIST and miR449a, which eventually influenced the expression of Bcl-2: XIST functioned as a miRNA sponge of miR-449a, which was a negative regulator of Bcl-2. These data show that expression of the lncRNA XIST is associated with an increased growth rate and metastatic potential in NSCLC A549 and NCI-H1299 cells partially through miR-449a, and suggest that XIST may be a potential prognostic factor and therapeutic target for patients with NSCLC.

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Section: Discussionmentioning

confidence: 96%

Section: Acta Pharmacologica Sinicamentioning

confidence: 99%

The lncRNA XIST exhibits oncogenic properties via regulation of miR-449a and Bcl-2 in human non-small cell lung cancer

Zhang

Hou

et al. 2017

Acta Pharmacol Sin

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“…Xist expression can be up-regulated in glioblastoma cells of both sexes and its knockdown results in tumour-suppression 108 . In testicular tumors, increased Xist expression is also frequently observed, which is not coupled with methylation of X linked genes, indicating that its role may be distinct from this process 109 .…”

Section: A) X Chromosomementioning

confidence: 99%

Sexual dimorphism in cancer

et al. 2016

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The incidence of many cancer types is significantly higher in the male than female populations, with associated differences in survival. Occupational and/or behavioral factors are well known underlying determinants. However, cellular/molecular differences between the two sexes are also likely to be important. We are focusing here on the complex interplay that sexual hormones and sex chromosomes can have in intrinsic control of cancer initiating cell populations, tumor microenvironment and systemic determinants of cancer development like the immune system and metabolism. A better appreciation of these differences between the two sexes could be of substantial value for cancer prevention as well as treatment.3 Introduction (Epidemiology)

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“…LncRNAs have emerged as new players in cancer research and several studies has shown that some lncRNAs function as oncogenes, tumor suppressor genes or both, depending on the circumstance [9]. X-inactive specific transcript (XIST), one of the novel-found LncRNA, has been confirmed that dysfunctional expression has a pathological role in cancer [10]. LncRNA XIST can act as a predictive biomarker for screening non-small lung cancer [11].…”

Section: Introductionmentioning

confidence: 99%

The Long Non-Coding RNA XIST Interacted with MiR-124 to Modulate Bladder Cancer Growth, Invasion and Migration by Targeting Androgen Receptor (AR)

Xiong

Wang

et al. 2017

Cell Physiol Biochem

102

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Backgrounds/Aims: Long non-coding RNA (lncRNA) X-inactive specific transcript (XIST) is involved in the progression of several tumors. The interaction between lncRNA and miRNA or miRNA’s target genes is reported to play crucial roles in malignancy. In addition, Androgen receptor (AR) is considered to be involved in bladder cancer progression. In this study, we investigated the role of XIST in human bladder cancer and its interaction with miR-124 and AR. Methods: XIST and AR expression was detected in bladder tumor samples and cell lines. Effects of XIST and AR on bladder cancer cells growth, invasion and migration were analyzed. Bioinformatic analysis and luciferase assays were used to identify the interaction among XIST, AR and miR-124. The correlations of miR-124 with XIST and AR in bladder cancer samples were statistically analyzed. Results: XIST and AR were upregulated in bladder cancer tissues and positively correlated. Higher XIST and AR expression were related to poorer TNM stage of bladder cancer. XIST knockdown reduced bladder cancer cells’ proliferation, invasion and migration. While this inhibitory effect could be partially restored by AR overexpression. XIST inhibited miR-124 expression by directly targeting. Moreover, miR-124 could bind to the 3’UTR of AR to regulate its expression. MiR-124 inhibition partially restored the XIST knockdown-induced reduction of AR, c-myc, p27, MMP13 and MMP9 expression. In bladder cancer tissues, miR-124 level was inversely correlated with the expression of XIST and AR, respectively. Conclusion: These findings indicated that XIST might be an oncogenic lncRNA that promoted the bladder cancer growth, invasion and migration via miR-124 dependent AR regulation.

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Knockdown of long non-coding RNA XIST exerts tumor-suppressive functions in human glioblastoma stem cells by up-regulating miR-152

Cited by 323 publications

References 45 publications

The lncRNA XIST exhibits oncogenic properties via regulation of miR-449a and Bcl-2 in human non-small cell lung cancer

The lncRNA XIST exhibits oncogenic properties via regulation of miR-449a and Bcl-2 in human non-small cell lung cancer

Sexual dimorphism in cancer

The Long Non-Coding RNA XIST Interacted with MiR-124 to Modulate Bladder Cancer Growth, Invasion and Migration by Targeting Androgen Receptor (AR)

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