miR‑106b‑5p promotes cell proliferation and cell cycle progression by directly targeting CDKN1A in osteosarcoma

He, Chuan; Chen, Hongwei; Liu, Yan; Li, Xin; Zhang, Chaoju; Qin, Qunyan; Pang, Qixiong

doi:10.3892/etm.2020.8574

Cited by 9 publications

(9 citation statements)

References 35 publications

(35 reference statements)

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“…Knowledge of the regulation and function of CDKN1A in cancer cells has opened up several areas of investigation and led to novel therapeutic strategies. Some miRNAs have been identified to be associated with CDKN1A expression [ 33–35 ]. The direct binding between miR-520h with CDKN1A was verified by dual-luciferase activity.…”

Section: Discussionmentioning

confidence: 99%

Over-expression of long non-coding RNA insulin-like growth factor 2-antisense suppressed hepatocellular carcinoma cell proliferation and metastasis by regulating the microRNA-520h/cyclin-dependent kinase inhibitor 1A signaling pathway

Huang

et al. 2021

Bioengineered

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Section: Discussionmentioning

confidence: 99%

Over-expression of long non-coding RNA insulin-like growth factor 2-antisense suppressed hepatocellular carcinoma cell proliferation and metastasis by regulating the microRNA-520h/cyclin-dependent kinase inhibitor 1A signaling pathway

Huang

et al. 2021

Bioengineered

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“…In total, 27 miRNAs were simultaneously identified from the two data sets. MiR-106b-5p, 24 miR-130a-3p, 25 miR-130b-3p, 26 miR-17-5p, 27 miR-19a-3p, 28 miR-19b-3p, 29 miR-301a-3p, 30 miR-4295, 31 and miR-93-5p 32 have been previously shown to be upregulated in OS and play oncogenic roles during cancer progression. In addition, no studies have reported an association of miR-1180-5p, miR-301b-3p, miR-3666, miR-519b-3p, miR-519c-3p, miR-520g-3p, miR-520h, miR-5590-3p, and miR-7114-3p with OS.…”

Section: Linc00839 Acts As a Sponge For Mir-454-3p In Os Cellsmentioning

confidence: 99%

<p>Long Noncoding RNA LINC00839 Promotes the Malignant Progression of Osteosarcoma by Competitively Binding to MicroRNA-454-3p and Consequently Increasing c-Met Expression</p>

Yang¹,

Guo²,

Ma³

et al. 2020

CMAR

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This study was conducted to determine the expression and prognostic relevance of long intergenic non-protein coding RNA 839 (LINC00839) in osteosarcoma (OS) and to explore the detailed roles of LINC00839 in regulating OS cell activities and the mechanisms responsible for its cancer-promoting activity in OS. Methods: The expression of LINC00839 in OS tissues and cell lines was determined by quantitative reverse transcription-polymerase chain reaction. After LINC00839 knockdown, cell counting kit-8 assay, flow cytometric analysis, transwell migration and invasion assay, and in vivo tumor xenograft assay were used to detect its effects on cellular processes in OS. Bioinformatics analyses were conducted to predict the putative miRNAs that target LINC00839. RNA immunoprecipitation assay, luciferase reporter assay, Western blotting analysis, and rescue assays were conducted to establish a relationship among LINC00839, microRNA-454-3p (miR-454-3p), and cellular mesenchymal to epithelial transition factor (c-Met) in OS. Results: LINC00839 was upregulated in OS tissues and cell lines. OS patients characterized with high LINC00839 expression exhibited shorter overall survival than patients with low LINC00839 expression. LINC00839 knockdown caused a significant reduction in OS cell proliferation, migration, and invasion in vitro. Furthermore, LINC00839 depletion inhibited OS tumor growth in vivo and induced apoptosis. Mechanistically, LINC00839 functions as a competitive endogenous RNA in OS by sponging miR-454-3p. c-Met was confirmed as a direct target gene for miR-454-3p in OS cells and was positively regulated by LINC00839 by competitively binding to miR-454-3p. Conclusion: LINC00839 promoted the oncogenicity of OS by targeting the miR-454-3p/ c-Met axis. The LINC00839/miR-454-3p/c-Met network may represent a potential target for OS therapy.

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“…BAK localizes to mitochondria, and functions to induce apoptosis. HDAC6 is involved in cell cycle and apoptosis [ 56 ], and CDKN1A and CDK members were critical in cell cycle progression [ 57 , 58 , 59 ]. Therefore, our results suggested that Tucidinostat and DL-sulforaphane suppressed the uLMS proliferation via cell cycle arrest and apoptosis.…”

Section: Resultsmentioning

confidence: 99%

Targeting Class I Histone Deacetylases in Human Uterine Leiomyosarcoma

Yang

Falahati

Khosh

et al. 2022

Cells

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Uterine leiomyosarcoma (uLMS) is the most frequent subtype of uterine sarcoma that presents a poor prognosis, high rates of recurrence, and metastasis. Currently, the molecular mechanism of the origin and development of uLMS is unknown. Class I histone deacetylases (including HDAC1, 2, 3, and 8) are one of the major classes of the HDAC family and catalyze the removal of acetyl groups from lysine residues in histones and cellular proteins. Class I HDACs exhibit distinct cellular and subcellular expression patterns and are involved in many biological processes and diseases through diverse signaling pathways. However, the link between class I HDACs and uLMS is still being determined. In this study, we assessed the expression panel of Class I HDACs in uLMS and characterized the role and mechanism of class I HDACs in the pathogenesis of uLMS. Immunohistochemistry analysis revealed that HDAC1, 2, and 3 are aberrantly upregulated in uLMS tissues compared to adjacent myometrium. Immunoblot analysis demonstrated that the expression levels of HDAC 1, 2, and 3 exhibited a graded increase from normal and benign to malignant uterine tumor cells. Furthermore, inhibition of HDACs with Class I HDACs inhibitor (Tucidinostat) decreased the uLMS proliferation in a dose-dependent manner. Notably, gene set enrichment analysis of differentially expressed genes (DEGs) revealed that inhibition of HDACs with Tucidinostat altered several critical pathways. Moreover, multiple epigenetic analyses suggested that Tucidinostat may alter the transcriptome via reprogramming the oncogenic epigenome and inducing the changes in microRNA-target interaction in uLMS cells. In the parallel study, we also determined the effect of DL-sulforaphane on the uLMS. Our study demonstrated the relevance of class I HDACs proteins in the pathogenesis of malignant uLMS. Further understanding the role and mechanism of HDACs in uLMS may provide a promising and novel strategy for treating patients with this aggressive uterine cancer.

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miR‑106b‑5p promotes cell proliferation and cell cycle progression by directly targeting CDKN1A in osteosarcoma

Cited by 9 publications

References 35 publications

Over-expression of long non-coding RNA insulin-like growth factor 2-antisense suppressed hepatocellular carcinoma cell proliferation and metastasis by regulating the microRNA-520h/cyclin-dependent kinase inhibitor 1A signaling pathway

Over-expression of long non-coding RNA insulin-like growth factor 2-antisense suppressed hepatocellular carcinoma cell proliferation and metastasis by regulating the microRNA-520h/cyclin-dependent kinase inhibitor 1A signaling pathway

<p>Long Noncoding RNA LINC00839 Promotes the Malignant Progression of Osteosarcoma by Competitively Binding to MicroRNA-454-3p and Consequently Increasing c-Met Expression</p>

Targeting Class I Histone Deacetylases in Human Uterine Leiomyosarcoma

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