Knockdown long non-coding RNA PEG10 inhibits proliferation, migration and invasion of glioma cell line U251 by regulating miR-506

Liang, Jinsong; Liu, Nina; Xin, Haibin

doi:10.4149/gpb_2019018

Cited by 14 publications

(6 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…For example, Troponin T3 (Tnnt3) as well as the Coiled-Coil Domain Containing Protein 80 (CCdc80), Alpha-3-Catenin (Ctnna3), and the Polycomb Group Ring Finger Protein (Pcgf5) play critical roles in cardiac/myogenic cell lineages and are crucial for striated muscle contraction [ 42 – 46 ]. Additionally, Zinc Finger Matrin-Type 4 (Zmat4) and the Paternally Expressed Gene 10 (Peg10) are implicated in mammalian neurogenesis [ 47 , 48 ], suggesting that VPA treatment induces changes in chromatin accessibility that favor onset of cell differentiation. This notion is supported by the fact that VPA exposure led to a net loss of ATAC-seq peaks and hence decreased accessibility at 3923 loci (Fig.…”

Section: Resultsmentioning

confidence: 99%

Changes in chromatin accessibility landscape and histone H3 core acetylation during valproic acid-induced differentiation of embryonic stem cells

Baumann

Zhang

Zhu

et al. 2021

Epigenetics & Chromatin

View full text Add to dashboard Cite

Directed differentiation of mouse embryonic stem cells (mESCs) or induced pluripotent stem cells (iPSCs) provides powerful models to dissect the molecular mechanisms leading to the formation of specific cell lineages. Treatment with histone deacetylase inhibitors can significantly enhance the efficiency of directed differentiation. However, the mechanisms are not well understood. Here, we use CUT&RUN in combination with ATAC-seq to determine changes in both histone modifications and genome-wide chromatin accessibility following valproic acid (VPA) exposure. VPA induced a significant increase in global histone H3 acetylation (H3K56ac), a core histone modification affecting nucleosome stability, as well as enrichment at loci associated with cytoskeletal organization and cellular morphogenesis. In addition, VPA altered the levels of linker histone H1 subtypes and the total histone H1/nucleosome ratio indicative of initial differentiation events. Notably, ATAC-seq analysis revealed changes in chromatin accessibility of genes involved in regulation of CDK serine/threonine kinase activity and DNA duplex unwinding. Importantly, changes in chromatin accessibility were evident at several key genomic loci, such as the pluripotency factor Lefty, cardiac muscle troponin Tnnt2, and the homeodomain factor Hopx, which play critical roles in cardiomyocyte differentiation. Massive parallel transcription factor (TF) footprinting also indicates an increased occupancy of TFs involved in differentiation toward mesoderm and endoderm lineages and a loss of footprints of POU5F1/SOX2 pluripotency factors following VPA treatment. Our results provide the first genome-wide analysis of the chromatin landscape following VPA-induced differentiation in mESCs and provide new mechanistic insight into the intricate molecular processes that govern departure from pluripotency and early lineage commitment.

show abstract

Section: Resultsmentioning

confidence: 99%

Changes in chromatin accessibility landscape and histone H3 core acetylation during valproic acid-induced differentiation of embryonic stem cells

Baumann

Zhang

Zhu

et al. 2021

Epigenetics & Chromatin

View full text Add to dashboard Cite

show abstract

“…Among the predicted miRNAs, we focused on miR-506 based on previous studies showing that miR-506 is involved in the biological processes of glioma. 21,22 Then, the results of luciferase activity and RNA pulldown assays led us to conclude that miR-506 is a target gene of LINC00963. LINC00963 and miR-506 were negatively regulated by each other in glioma cells, and they were inversely correlated in tumor tissues.…”

Section: Discussionmentioning

confidence: 99%

“…Meanwhile, our data indicated the tumor suppressor role of miR-506 in glioma pathogenesis owing to its suppressive effect on cell growth, migration, and invasion, which was similar to previous studies. 21,22 Furthermore, miR-506 inhibits cell proliferation, adhesion, and invasion in breast cancer cells by inactivating IQGAP1 and its downstream ERK/MAPK signaling pathways. 23 Ectopic expression of miR-506 suppressed epithelial-to-mesenchymal transition and angiogenesis in gastric cancer.…”

Section: Discussionmentioning

confidence: 99%

<p>LINC00963 Confers Oncogenic Properties in Glioma by Regulating the miR-506/BCAT1 Axis</p>

Ye¹,

Xu²,

Ge³

et al. 2020

CMAR

View full text Add to dashboard Cite

Background: Glioma is a prevalent disease of the central nervous system with a high incidence and mortality rate. Many long noncoding RNAs (lncRNAs) have been determined to be critical regulators of glioma oncogenesis. However, the function and mechanism of LINC00963 in glioma have not been fully elucidated. Methods: The expression level of RNA was determined by qRT-PCR, and the protein level was determined by Western blot analysis. A luciferase activity assay was conducted to verify the interaction between miRNA and lncRNA or the target gene. The proliferation, cell cycle distribution, invasion, and migration were evaluated by MTT, EdU, flow cytometry, woundhealing and Transwell invasion assays, respectively. In vivo tumor growth was evaluated in a xenograft nude mouse model. Results: We found that LINC00963 was upregulated in glioma cells and tissues and associated with the poor prognosis of patients with glioma. Ectopic expression of LINC00963 promoted cell proliferation, cell cycle progression, migration, and invasion in vitro and tumorigenesis in vivo. Mechanistically, the results of luciferase activity and RNA pulldown assays validated that LINC00963 could act as a molecular sponge of miR-506. Reciprocal repression was found between LINC00963 and miR-506. In addition, BCAT1 was identified as a target of miR-506, and both the mRNA and protein levels of BCAT1 were reduced by miR-506. In tumor tissues, the expression of BCAT1 was negatively and positively correlated with miR-506 and LINC00963 expression, respectively. The reintroduction of BCAT1 in glioma cells abolished the tumor suppressive function of miR-506 by promoting cell viability and motility. The upregulated LINC00963 and BCAT1 were associated with the aggressive phenotypes of tumors. Conclusion: Our data revealed that LINC00963 confers oncogenic function in the progression of glioma and that the LINC00963/miR-506/BCAT1 axis may be a novel mechanism and therapeutic strategy for this disease.

show abstract

“…In addition, some lncRNAs can affect the expression of STAT3 without a clear and specific mechanism. For example, knockdown of lncRNA PEG10 inhibited U251 cell proliferation, migration, and invasion and inactivated the Raf/MEK/ERK and JAK1/STAT3 signalling pathways by increasing miR-506 expression [ 90 ]. In addition, lncRNA gastric carcinoma highly expressed transcript 1 (GHET1), acting as an oncogene; promoted cell proliferation, migration, and invasion; and activated the JAK2/STAT3 and p53/survivin signalling pathways by miR-216a downregulation [ 91 ].…”

Section: Lncrnas Are Involved In the Stat3 Signalling Pathwaymentioning

confidence: 99%

Noncoding RNAs involved in the STAT3 pathway in glioma

Zheng

et al. 2021

Cancer Cell Int

View full text Add to dashboard Cite

Glioma is the most common malignant primary brain tumour in adults. Despite improvements in neurosurgery and radiotherapy, the prognosis of glioma patients remains poor. One of the main limitations is that there are no proper clinical therapeutic targets for glioma. Therefore, it is crucial to find one or more effective targets. Signal transducer and activator of transcription 3 (STAT3) is a member of the STAT family of genes. Abnormal expression of STAT3 is involved in the process of cell proliferation, migration, invasion, immunosuppression, angiogenesis, dryness maintenance, and resistance to radiotherapy and chemotherapy in glioma. Therefore, STAT3 has been considered an ideal therapeutic target in glioma. Noncoding RNAs (ncRNAs) are a group of genes with limited or no protein-coding capacity that can regulate gene expression at the epigenetic, transcriptional and posttranscriptional level. In this review, we summarized the ncRNAs that are correlated with the ectopic expression of STAT3 in glioma.

show abstract

Knockdown long non-coding RNA PEG10 inhibits proliferation, migration and invasion of glioma cell line U251 by regulating miR-506

Cited by 14 publications

References 33 publications

Changes in chromatin accessibility landscape and histone H3 core acetylation during valproic acid-induced differentiation of embryonic stem cells

Changes in chromatin accessibility landscape and histone H3 core acetylation during valproic acid-induced differentiation of embryonic stem cells

<p>LINC00963 Confers Oncogenic Properties in Glioma by Regulating the miR-506/BCAT1 Axis</p>

Noncoding RNAs involved in the STAT3 pathway in glioma

Contact Info

Product

Resources

About