Long noncoding RNA XIST acts as an oncogene in non-small cell lung cancer by epigenetically repressing KLF2 expression

Fang, Jing; Sun, Chengcao; Chen, Gong

doi:10.1016/j.bbrc.2016.08.030

Cited by 196 publications

(164 citation statements)

References 47 publications

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“…Moreover, siRNA knock down of XIST could repress cell proliferation, invasion and migration of TCC-SUP and UM-UC-3 cells; the inhibitory effect of si-XIST on cell proliferation, invasion and migration could be partially restored by pCMV-AR transfection. These results suggested that XIST and AR functions as oncogenes in bladder cancer, consistent with the results from Fang et al that XIST acts as an oncogene in non-small cell lung cancer [37], and the results from Zhang et al that AR mediates proliferation of breast cancer cells [42]. Further experiments were performed to investigate the underlying mechanism by which XIST regulate AR expression and exerts its effect on bladder cancer cell proliferation, invasion and migration.…”

Section: Discussionsupporting

confidence: 74%

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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Section: Discussionsupporting

confidence: 74%

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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“…Among them, 33 studies involved participants from China [11–43] and three studies involved patients respectively from Japan [44], Germany [45] and USA [46]. All studies investigated patients with NSCLC and qRT–PCR was used to detect lncRNAs expression in tumor tissues.…”

Section: Resultsmentioning

confidence: 99%

The prognostic value of long non coding RNAs in non small cell lung cancer: A meta-analysis

Wang

Zhu

et al. 2016

Oncotarget

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Background Reports have demonstrated the prognostic function of long non-coding RNAS (lncRNAS) in patients with cancer. However, their prognostic functions in non small cell lung cancer (NSCLC) remain controversial. We therefore performed a meta-analysis on six lncRNAs (PVT1, AFAP1-AS1, LINC01133, ANRIL, MEG3 and UCA1) to clarify their prognostic roles in NSCLC. Results Thirty-six studies involving 6267 patients with NSCLC and 34 lncRNAs were included. Of the listed lncRNAs, 20 were shown to negatively affect patients' overall survival while the high expression of 13 lncRNAs indicated better survival outcomes. Materials and Methods The log-rank p value and Kaplan–Meier survival curves of survival outcomes were extracted for hazard ratio (HR) calculation. Survival outcomes were measured by overall survival (OS) and event free survival (EFS) which were then analyzed by calculating pooled hazard ratios. The heterogeneity was detected by Q statistic and I-squared statistic. Conclusions The abnormal expression of lncRNAs may significantly affect NSCLC patients' survival and may serve as a novel predictive factor for prognosis of NSCLC patients.

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“…Total proteins were extracted from cultured cells using RIPA buffer containing PMSF and quantified using BCA protein assay kit (Beyotime, Haimen, China)[18–22]. Protein lysates were subjected to SDS-PAGE and transferred onto polyvinylidenedifluoride (PVDF) membrane (Millipore, Billerica, MA) followed by incubating with a primary antibody, and then a secondary antibody.…”

Section: Methodsmentioning

confidence: 99%

Long non-coding RNA EWSAT1 promotes human nasopharyngeal carcinoma cell growth in vitro by targeting miR-326/-330-5p

Song

Yin

2016

Aging

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Long non-coding RNA (lncRNA) Ewing sarcoma associated transcript 1 (EWSAT1) has been identified as an oncogene, and its dysregulation is closed corrected with tumor progression in Ewing sarcoma. Recently, high-through put analysis reveals that EWSAT1 is also highly expressed in human nasopharyngeal carcinoma (NPC). However, whether the aberrant expression of EWSAT1 in NPC is corrected with malignancy or prognosis has not been expounded. Herein, we identified that EWSAT1 was up-regulated in NPC tissues and cell lines, and higher expression of EWSAT1 resulted in a markedly poorer survival time. EWSAT1 over-expression facilitated, while EWSAT1 silencing impaired cell growth in NPC. In addition, mechanistic analysis demonstrated that EWSAT1 up-regulated the expression of miR-326/330-5p clusters targeted gene cyclin D1 through acting as a competitive ‘sponge’ of miR-326/330-5p clusters. Collectively, our data revealed that EWSAT1 promotes NPC cell growth in vitro through up-regulating cyclin D1 partially via ‘spongeing’ miR-326/330-5p clusters.

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Long noncoding RNA XIST acts as an oncogene in non-small cell lung cancer by epigenetically repressing KLF2 expression

Cited by 196 publications

References 47 publications

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

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

The prognostic value of long non coding RNAs in non small cell lung cancer: A meta-analysis

Long non-coding RNA EWSAT1 promotes human nasopharyngeal carcinoma cell growth in vitro by targeting miR-326/-330-5p

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