MicroRNA‑30a suppresses non‑small‑cell lung cancer by targeting Myb‑related protein B

Geng, Guannan; Yang, Ying‐Tao; Jiang, Jie; Yu, Xin; Fa, Xianen

doi:10.3892/etm.2017.5559

Cited by 13 publications

(16 citation statements)

References 36 publications

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“…MYBL2 and TFDP1 are targeted by five common miRNAs (hsa-miR-30a-5p, hsa-miR-30b-5p, hsa-miR-30c-5p, hsa-miR-30d-5p, hsa-miR-30e-5p), though they belong from same miRNA family. A previous study showed the down-regulation of hsa-miR-30a-5p which directly targeting MYBL2 mRNA in NSCLC (93). Interestingly, TCGA NSCLC dataset showed higher mutation rates in the genes of “driver-network” as well as its upstream regulators FOXM1 and MYBL1 in the NSCLC (Figure 6).…”

Section: Discussionmentioning

confidence: 97%

Integrated Network Analysis Reveals FOXM1 and MYBL2 as Key Regulators of Cell Proliferation in Non-small Cell Lung Cancer

Ahmed

2019

Front. Oncol.

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Background: Loss of control on cell division is an important factor for the development of non-small cell lung cancer (NSCLC), however, its molecular mechanism and gene regulatory network are not clearly understood. This study utilized the systems bioinformatics approach to reveal the “driver-network” involve in tumorigenic processes in NSCLC.Methods: A meta-analysis of gene expression data of NSCLC was integrated with protein-protein interaction (PPI) data to construct an NSCLC network. MCODE and iRegulone were used to identify the local clusters and its upstream transcription regulators involve in NSCLC. Pair-wise gene expression correlation was performed using GEPIA. The survival analysis was performed by the Kaplan-Meier plot.Results: This study identified a local “driver-network” with highest MCODE score having 26 up-regulated genes involved in the process of cell proliferation in NSCLC. Interestingly, the “driver-network” is under the regulation of TFs FOXM1 and MYBL2 as well as miRNAs. Furthermore, the overexpression of member genes in “driver-network” and the TFs are associated with poor overall survival (OS) in NSCLC patients.Conclusion: This study identified a local “driver-network” and its upstream regulators responsible for the cell proliferation in NSCLC, which could be promising biomarkers and therapeutic targets for NSCLC treatment.

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Section: Discussionmentioning

confidence: 97%

Integrated Network Analysis Reveals FOXM1 and MYBL2 as Key Regulators of Cell Proliferation in Non-small Cell Lung Cancer

Ahmed

2019

Front. Oncol.

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“…In this study, we showed that miR‐30a is involved in the proliferation of AI cells by targeting MYBL2, FOXD1, and SOX4, and the schematic diagram was shown in Figure 6F. MYBL2 previously had been reported as miR‐30a target in acute myeloid leukemia 42 and non–small‐cell lung cancer 43 . FOXD1 was also a miR‐30a target in human ovarian carcinoma 44 and osteosarcoma 45 .…”

Section: Discussionmentioning

confidence: 62%

miR‐30a inhibits androgen‐independent growth of prostate cancer via targeting MYBL2, FOXD1, and SOX4

et al. 2020

The Prostate

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Background: Castrate-resistant prostate cancer (CRPC) is an aggressive and lethal disease. The pathogenesis of CRPC is not fully understood and novel therapeutic targets need to be identified to improve the patients' prognosis. has been demonstrated to be a tumor suppressor in many types of solid malignancies. However, its role in androgen-independent (AI) growth of prostate cancer (PCa) received limited attention as yet. Methods:The clinical association of miR-30a and its potential targets with AI growth was characterized by bioinformatics analyses. Regulation of cell proliferation and colony formation rates by miR-30a were tested using PCa cell models. Xenograft models were used to measure the regulation of prostate tumor growth by miR-30a.The real-time quantitative polymerase chain reaction was used to validate whether miR-30a and its targets regulate cell cycle control genes and androgen receptor (AR)-dependent transcription. Bioinformatics tools, Western blot, and luciferase reporter assays were utilized to identify miR-30a targets. Results: Bioinformatic analysis showed that low expression of miR-30a is associated with castration resistance of PCa patients and poor outcomes. Transfection of miR-30a mimics inhibited the AI growth of PCa cells in vitro and in vivo. Upregulation of miR-30a in 22RV1 cells altered the expression of cell cycle control genes and AR-mediated transcription, while downregulation of miR-30a in LNCaP cells had the opposite effects to AR-mediated transcription. MYBL2, FOXD1, and SOX4 were identified as miR-30a targets. Downregulation of MYBL2, FOXD1, and SOX4 affected the expression of cell cycle control genes and AR-mediated transcription and suppressed the AI growth of 22RV1 cells. Conclusions: Our results suggest that miR-30a inhibits AI growth of PCa by targeting MYBL2, FOXD1, and SOX4. They provide novel insights into developing new treatment strategies for CRPC. K E Y W O R D S castration-resistant prostate cancer, FOXD1, miR-30a, MYBL2, SOX4

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“…Studies have also showed that miR-30a induces cell cycle arrest. Overexpression of miR-30a increases cell apoptosis and induces cell cycle arrest in non-small cell lung cancer (38). miR-30a has also been demonstrated to promote cell cycle arrest at the G1 phase (39).…”

Section: Discussionmentioning

confidence: 99%

Rapamycin‑induced miR‑30a downregulation inhibits senescence of VSMCs by targeting Beclin1

et al. 2019

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Vascular senescence is considered to be an independent risk factor for cardiovascular diseases. The present study aimed to investigate the effects of rapamycin on miR-30a and its relationship with autophagy and senescence in vascular smooth muscle cells (VSMCs). Young and aging VSMCs were treated with rapamycin or transfected with miR-30a mimics. Measurement of cellular senescence was conducted using senescence-associated (SA)-β-Galactosidase (gal) staining. Dual luciferase reporter assay was used to confirm binding for miR-30a and Beclin1. The expression levels of miR-30a and Beclin1 were determined with reverse transcription-quantitative polymerase chain reaction analysis. Autophagy-related protein levels were determined using immunofluorescence or western blot assays. The results demonstrated that rapamycin treatment significantly decreased miR-30a expression and increased Beclin1 expression in both young and aging cells, as well as promoted autophagy in VSMCs. In addition, rapamycin inhibited senescence in VSMCs and could also alleviate the aging VSMC cycle arrest. Dual luciferase reporter assay confirmed that miR-30a could directly bind the 3′untranslated region of Beclin1 and inhibit its expression. Furthermore, miR-30a inhibited autophagy and promoted senescence of VSMCs. In conclusion, the present results indicated that rapamycin could inhibit the senescence of VSMCs by downregulating miR-30a, which resulted in upregulation of Beclin1 and activation of autophagy. The current study is the first to demonstrate an inhibitory role of rapamycin on VSMC senescence and might provide novel insights and potential new molecular targets in senescence treatment.

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MicroRNA‑30a suppresses non‑small‑cell lung cancer by targeting Myb‑related protein B

Cited by 13 publications

References 36 publications

Integrated Network Analysis Reveals FOXM1 and MYBL2 as Key Regulators of Cell Proliferation in Non-small Cell Lung Cancer

Integrated Network Analysis Reveals FOXM1 and MYBL2 as Key Regulators of Cell Proliferation in Non-small Cell Lung Cancer

miR‐30a inhibits androgen‐independent growth of prostate cancer via targeting MYBL2, FOXD1, and SOX4

Rapamycin‑induced miR‑30a downregulation inhibits senescence of VSMCs by targeting Beclin1

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