lncRNA XIST promotes glioma proliferation and metastasis through miR‑133a/SOX4

Luo, Chixing; Quan, Zhongping; Zhong, Balian; Zhang, Ming; Zhou, Bo; Wang, Shaobo; Luo, Xinkai; Tang, Changjiu

doi:10.3892/etm.2020.8426

Cited by 30 publications

(23 citation statements)

References 35 publications

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“… 24 The anti-proliferatory (decreased by 20.51 ± 2.43% and 19.76 ± 1.85%, 70.42 ± 6.91% and 66.39 ± 6.53%, as well as 69.42 ± 7.68% and 63.66 ± 6.59% at the 24th, 48th h, and 72nd h, respectively), anti-invasive (from 96.55 ± 8.57 to 35.38 ± 4.19 and from 129.26 ± 11.12 to 45.63 ± 4.15), anti-migratory (from 136.25 ± 15.42 to 41.74 ± 5.26 and from 158.97 ± 16.23 to 53.36 ± 7.48) and pro-apoptotic (from 8.14 ± 0.82% to 26.45 ± 2.65% and from 6.93 ± 0.71% to 23.91 ± 2.36%) properties of miR-133a have been underscored in further functional experiments in A549 and H1299 cells. More importantly, the anti-metastatic role of miR-133a in vivo has also been highlighted in glioma 25 and gastric cancer, 26 which were largely consistent with our results.…”

Section: Discussionsupporting

confidence: 91%

KDM5C Expedites Lung Cancer Growth and Metastasis Through Epigenetic Regulation of MicroRNA-133a

Zhang¹,

Liu²,

Wang³

et al. 2021

OTT

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Background KDM5C, a histone H3K4-specific demethylase, possess various biological functions in development of cancers. However, its relation to the microRNA (miRNA) regulation in lung cancer remains unknown. This study aims to study the regulatory role of KDM5C on modification of miR-133a in the progression of lung cancer. Methods Differentially expressed miRNAs were filtered from 34 paired lung cancer and paracancerous tissues. The correlation between miR-133a expression and the prognosis of lung cancer patients was determined by a bioinformatics website. Furthermore, malignant aggressiveness of lung cancer cells was detected after miR-133a upregulation by CCK-8, flow cytometry, and Transwell assays and in vivo tumorigenesis and metastasis experiments. Subsequently, we analyzed mRNA downregulated in cells overexpressing miR-133a using m microarray analysis and expounded the upstream regulatory mechanism of miR-133a using bioinformatics website prediction and functional validation. Results miR-133a was reduced in lung cancer tissues, and patients with low expression of miR-133a have worse survival rates. miR-133a restoration curtailed growth and metastasis of lung cancer cells in vitro and in vivo. Moreover, miR-133a downregulated PTBP1 expression, whereas overexpression of PTBP1 attenuated the suppressive effect of miR-133a on lung cancer cell aggressiveness. The level of methylation modification of miR-133a was reduced in lung cancer cells. KDM5C inhibited the expression of miR-133a by promoting the demethylation modification of its promoter histone. Conclusion Histone demethylase KDM5C inhibits the expression of miR-133a by elevating the demethylation modification of the promoter histone of miR-133a, thereby promoting the expression of PTBP1, which finally accelerates lung cancer cell growth and metastasis.

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Section: Discussionsupporting

confidence: 91%

KDM5C Expedites Lung Cancer Growth and Metastasis Through Epigenetic Regulation of MicroRNA-133a

Zhang¹,

Liu²,

Wang³

et al. 2021

OTT

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“…And miR-133a can function as a regulator of cancer metastasis by targeting SOX4, MMP9, etc. 34 , 35 . This study focused on the regulatory effect of miR-133a on GEF-H1 /RhoA, and tended to add a new branch to its regulatory network.…”

Section: Discussionmentioning

confidence: 99%

Hypoxia induced exosomal circRNA promotes metastasis of Colorectal Cancer via targeting GEF-H1/RhoA axis

et al. 2020

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Hypoxia is one of the important properties of solid tumor. However, oxygen supply within tumors is generally heterogeneous according to the distance from the nearest blood vessel. The discrepancy of metastatic potential exists between hypoxic cancer cells and relatively normoxic cancer cells. But the molecular mechanism remains poorly understood. Methods: Differential expression of circRNAs in plasma exosomes of CRC patients and normal subjects was performed by screening. Exosomes were isolated by ultra-centrifugation and RNA expressions were determined by RT-qPCR. The migratory capacity of cells was performed by high intension imaging, wound healing assay and transwell chamber migration assay. Results: Circ-133 is enriched in the plasma exosomes of CRC patients and increased with the disease progression. Exosomal circ-133 derived from hypoxic cells delivered into normoxic cells and promoted cancer metastasis by acting on miR-133a/GEF-H1/RhoA axis. Meanwhile, animal experiments revealed that knockdown of circ-133 can inhibit tumor metastasis. Circ-133 is expected to be a new biomarker for monitoring tumor progression and might be a novel therapeutic target. Conclusions: Hypoxia-derived exosomal circ-133 transported into normaxic cancer cells and promoted cell migration via miR-133a/GEF-H1/RhoA axis. This study reveals a potential mechanism for that the intra-tumor heterogeneity of oxygen promote cancer progression.

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“…They observed negative regulation between XIST and miR-133a in glioma cell lines. Their study reported that overexpression of miR-133a prevented glioma cell proliferation, metastasis and EMT by reducing the expression of SOX4 [ 159 ]. Consistently, other miRNAs, such as miR-429 [ 160 ], miR-210 [ 161 ], miR-92b [ 162 ] and miR-204-5p [ 163 ] may also modulates the expression of XIST in gliomas.…”

Section: Overview Of Long Non-coding Rnas In Glioblastomamentioning

confidence: 99%

Potential of long non-coding RNAs as a therapeutic target and molecular markers in glioblastoma pathogenesis

Chaudhary

2021

Heliyon

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Glioblastoma (GB) is by far the most hostile type of malignant tumor that primarily affects the brain and spine, derived from star-shaped glial cells that are astrocytes and oligodendrocytes. Despite of significant efforts in recent years in glioblastoma research, the clinical efficacy of existing medical intervention is still limited and very few potential diagnostic markers are available. Long non-coding RNAs (lncRNAs) that lacks protein-coding capabilities were previously thought to be “junk sequences” in mammalian genomes are quite indispensible epigenetic regulators that can positively or negatively regulate gene expression and nuclear architecture, with significant roles in the initiation and development of tumors. Nevertheless, the precise mechanism of these distortedly expressed lncRNAs in glioblastoma pathogenesis is not yet fully understood. Since the advent of high-throughput sequencing technologies, more and more research have elucidated that lncRNAs are one of the most promising prognostic biomarkers and therapeutic targets for glioblastoma. In this paper, I briefly outlined the existing findings of lncRNAs. And also summarizes the profiles of different lncRNAs that have been broadly classified in glioblastoma research, with emphasis on both their prognostic and therapeutic values.

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lncRNA XIST promotes glioma proliferation and metastasis through miR‑133a/SOX4

Cited by 30 publications

References 35 publications

KDM5C Expedites Lung Cancer Growth and Metastasis Through Epigenetic Regulation of MicroRNA-133a

KDM5C Expedites Lung Cancer Growth and Metastasis Through Epigenetic Regulation of MicroRNA-133a

Hypoxia induced exosomal circRNA promotes metastasis of Colorectal Cancer via targeting GEF-H1/RhoA axis

Potential of long non-coding RNAs as a therapeutic target and molecular markers in glioblastoma pathogenesis

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