LncRNA XIST/miR-200c regulates the stemness properties and tumourigenicity of human bladder cancer stem cell-like cells

Xu, Ran; Zhu, Xuan; Chen, Fangzhi; Huang, Chí; Ai, Kai; Wu, Hongtao; Zhang, Lei; Zhao, Xiaokun

doi:10.1186/s12935-018-0540-0

Cited by 67 publications

(50 citation statements)

References 31 publications

(40 reference statements)

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“…10 Research have shown that lncRNAs play a significant role in many life activities, such as dose-compensating effects, 11 epigenetic regulation, 12 regulation of cell cycle, 13 and regulation of cell differentiation 14 and has become a focus of genetic research. 16,17 Some studies have shown that X-inactive specific transcript (XIST) can be involved in the occurrence of gastric cancer, bladder cancer, 18,19 but the specific mechanism of XIST in bladder cancer is still not clear. 16,17 Some studies have shown that X-inactive specific transcript (XIST) can be involved in the occurrence of gastric cancer, bladder cancer, 18,19 but the specific mechanism of XIST in bladder cancer is still not clear.…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA XIST participates in bladder cancer by downregulating p53 via binding to TET1

Shi

et al. 2018

J of Cellular Biochemistry

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Long noncoding RNAs (lncRNAs) have been reported to take part in intracellular RNA regulatory networks and play important roles in a lot of pathological processes. Currently, lncRNA X‐inactive specific transcript (XIST) has been proved to regulate cell migration, proliferation, and apoptosis in a series of cancers. In this study, we explored whether XIST can affect cell proliferation, migration, and apoptosis in bladder cancer. The influences of XIST on the cell proliferation, cell cycle, and apoptosis were detected in bladder cancer cells. The effect of XIST on the migration of bladder cancer cells was examined by cell migration assay. Through RNA immunoprecipitation and chromatin immunoprecipitation assays, the binding relationship between XIST and TET1 and the regulatory mechanism of TET1 on p53 were examined. Western blot was performed to detect p53 after knockdown or overexpression of XIST. We found that knockdown of XIST suppressed cell migration and proliferation in vitro. Mechanistically, we confirmed that lncRNA XIST participates in bladder cancer by downregulating p53 via binding to TET1. In conclusion, our research revealed the potential role of XIST‐TET1‐p53 regulatory network in bladder cancer.

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Section: Introductionmentioning

confidence: 99%

Long noncoding RNA XIST participates in bladder cancer by downregulating p53 via binding to TET1

Shi

et al. 2018

J of Cellular Biochemistry

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“…The results indicated that miR‐200c overexpression and XIST knockdown could prevent cell clone formation, self‐renewal ability, and EMT in BCSC‐like cells. miR‐200c knockdown could restore the tumor growth inhibition caused by XIST knockdown (R. Xu et al, ). Also, it is found that Knockdown of lncRNA XIST exerts tumor‐suppressive functions in human glioblastoma stem cells by upregulating miR‐152 (Yao et al, ).…”

Section: Diagnosis Prognosis and Therapeutic Implicationsmentioning

confidence: 99%

microRNAs in cancer stem cells: Biology, pathways, and therapeutic opportunities

Asadzadeh

Mansoori

Mohammadi

et al. 2018

Journal Cellular Physiology

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Cancer stem cells (CSCs) are a small subpopulation of tumor cells that have been identified in most types of cancer. Features that distinguish them from the bulk of tumor cells include their pluripotency, self‐renewal capacity, low proliferation rate, and tumor‐initiating ability. CSCs are highly malignant, as they confer drug resistance and facilitate tumor progression, relapse, and metastasis. The molecular mechanisms underlying CSC biology are now beginning to be understood. In this context, microRNAs (miRNAs) occupy a prominent place. These endogenous, small noncoding RNA molecules control gene expression at the posttranscriptional level. This study reviews our current understanding of how the misexpression of tumor suppressor and oncogenic miRNAs in CSCs sustain their abundance and malignant properties. We discuss how they partly do so by acting on major CSC signaling pathways, including the Wnt, Notch, Hedgehog, and BMI‐1 pathways. Our current knowledge of miRNA functions in CSCs may now be used for cancer diagnostic and prognostic purposes. In addition, when combined with recent technical advances in the in vivo delivery of miRNAs, we are now in an excellent position to develop strategies that harness miRNA interference and replacement technologies for the therapeutic targeting of CSCs.

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“…We report that lncRNA XIST (X-inactive-specific transcript), which is involved in genomic imprinting and the transcriptional silencing of genes on the X chromosome and is highly expressed in tumor tissues [11][12][13][14][15], is an epigenetic regulator targeted by miR-7 that directly bound and inhibited XIST expression in breast cancer by using the RNA in vivo precipitation (RIP) method, which underlies the attenuation of properties of BCSCs and the decrease of the BCSC subset. MiR-7 also modulated the miR-92b/Slug/ESA (epithelium-specific antigen) axis and reduced CD44 and Slug expression, resulting in a decrease in cancer cell stemness and the BCSC subset in breast cancer.…”

Section: Introductionmentioning

confidence: 99%

MiR-7 reduces the BCSC subset by inhibiting XIST to modulate the miR-92b/Slug/ESA axis and inhibit tumor growth

Pan

You

et al. 2020

Breast Cancer Res

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Background: Breast cancer stem cells (BCSCs) are typically seed cells of breast tumor that initiate and maintain tumor growth. MiR-7, as a cancer inhibitor, decreases the BCSC subset and inhibits tumor progression through mechanisms that remain unknown. Methods: We examined miR-7 expression in breast cancer and developed a BCSC-driven xenograft mouse model, to evaluate the effects of miR-7 overexpression on the decrease of the BCSC subset in vitro and in vivo. In addition, we determined how miR-7 decreased the BCSC subset by using the ALDEFLUOR, lentivirus infection, dual-luciferase reporter, and chromatin immunoprecipitation-PCR assays. Results: MiR-7 was expressed at low levels in breast cancer tissues compared with normal tissues, and overexpression of miR-7 directly inhibited lncRNA XIST, which mediates the transcriptional silencing of genes on the X chromosome, and reduced epithelium-specific antigen (ESA) expression by increasing miR-92b and inhibiting slug. Moreover, miR-7 suppressed CD44 and ESA by directly inhibiting the NF-κB subunit RELA and slug in breast cancer cell lines and in BCSC-driven xenografts, which confirmed the antitumor activity in mice injected with miR-7 agomir or stably infected with lenti-miR-7. Conclusions: The findings from this study uncover the molecular mechanisms by which miR-7 inhibits XIST, modulates the miR-92b/Slug/ESA axis, and decreases the RELA and CD44 expression, resulting in a reduced BCSC subset and breast cancer growth inhibition. These findings suggest a potentially targeted treatment approach to breast cancer.

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LncRNA XIST/miR-200c regulates the stemness properties and tumourigenicity of human bladder cancer stem cell-like cells

Cited by 67 publications

References 31 publications

Long noncoding RNA XIST participates in bladder cancer by downregulating p53 via binding to TET1

Long noncoding RNA XIST participates in bladder cancer by downregulating p53 via binding to TET1

microRNAs in cancer stem cells: Biology, pathways, and therapeutic opportunities

MiR-7 reduces the BCSC subset by inhibiting XIST to modulate the miR-92b/Slug/ESA axis and inhibit tumor growth

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