miR‐106b‐5p promotes aggressive progression of hepatocellular carcinoma via targeting RUNX3

Gu, Shensen; Zhang, Xinlong; Zhang, Song-Jiang; Zhang, Dongming; Lin, Junsheng; Hasengbayi, Saiken; Han, Wei

doi:10.1002/cam4.2511

Cited by 31 publications

(21 citation statements)

References 31 publications

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“…In this analysis, we focused on the top four OncoMMRs that had the largest number of targets (miR-106b-5p, miR-106a-5p, miR-671-5p, and miR-590-3p) ( Figure 6 ). The expression levels of this OncoMMRs have been widely associated with increased cell proliferation, migration, invasion, and radioresistance [ 41 , 42 , 43 , 44 , 45 , 46 ] showing concordance with our results. Moreover, the top-four OncoMMRs mentioned before were highly enriched in genes involved in invasion and metastasis, suggesting a co-participation in this hallmark.…”

Section: Discussionsupporting

confidence: 91%

Identification of miRNA Master Regulators in Breast Cancer

Martínez-Gutierrez

León

Millan-Catalan

et al. 2020

Cells

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Breast cancer is the neoplasm with the highest number of deaths in women. Although the molecular mechanisms associated with the development of this tumor have been widely described, metastatic disease has a high mortality rate. In recent years, several studies show that microRNAs or miRNAs regulate complex processes in different biological systems including cancer. In the present work, we describe a group of 61 miRNAs consistently over-expressed in breast cancer (BC) samples that regulate the breast cancer transcriptome. By means of data mining from TCGA, miRNA and mRNA sequencing data corresponding to 1091 BC patients and 110 normal adjacent tissues were downloaded and a miRNA–mRNA network was inferred. Calculations of their oncogenic activity demonstrated that they were involved in the regulation of classical cancer pathways such as cell cycle, PI3K–AKT, DNA repair, and k-Ras signaling. Using univariate and multivariate analysis, we found that five of these miRNAs could be used as biomarkers for the prognosis of overall survival. Furthermore, we confirmed the over-expression of two of them in 56 locally advanced BC samples obtained from the histopathological archive of the National Cancer Institute of Mexico, showing concordance with our previous bioinformatic analysis.

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Section: Discussionsupporting

confidence: 91%

Identification of miRNA Master Regulators in Breast Cancer

Martínez-Gutierrez

León

Millan-Catalan

et al. 2020

Cells

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“…According to a previous study [ 24 ], miR-106b-5p promotes malignant melanoma progression possibly through targeting PTEN to regulate cell cycle-related proteins and Akt/ERK signaling pathway. MiR-106b-5p plays a carcinogenic role in hepatocellular carcinoma through regulating the target gene RUNX3 [ 25 ]. In addition, a recent clinical study incorporating 284 renal carcinoma patients showed that the expression of miR-106b-5p is negatively correlated with the overall survival of the patients, moreover, the study also indicated that miR-106b-5p expression was an independent predictor of poor prognosis in renal carcinoma patients [ 26 ].…”

Section: Discussionmentioning

confidence: 99%

MiR-106b-5p regulates the migration and invasion of colorectal cancer cells by targeting FAT4

Pan¹,

Chen²,

Lu³

et al. 2020

Bioscience Reports

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MicroRNA-106b-5p (miR-106b-5p) is involved in the development of many cancers including in colorectal cancer (CRC), and FAT4 is correlated with regulation of growth and apoptosis of cancer cells. This study aimed to investigate the relation between FAT4 and miR-106b-5p and the underlying mechanism of the two on the development of CRC. Quantitative real-time PCR (qRT-PCR) assay and Western blot (WB) analysis were performed to detect the expressions of mRNAs, miRNA and proteins. The viability of CRC cells was detected by cell counting kit-8 (CCK-8). Scratch test and transwell assay were performed to measure the migration and invasion of CRC cell. Tumor angiogenesis was simulated by in vitro angiogenesis experiment. Dual-luciferase reporter assay was performed to verify the targeting relation between miR-106b-5p and FAT4. The study found that the expression of FAT4 was down-regulated and that of miR-106b-5p was up-regulated in CRC tissues. Overexpression of FAT4 resulted in decreased proliferation, migration, invasion and angiogenesis of CRC cells, whereas silencing of FAT4 led to the opposite results. In rescue experiment, miR-106b-5p partially reversed the function of FAT4 in CRC cells, thus playing a carcinogenic role by targeting FAT4 in the CRC cells.

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“…Additionally, a previous study has revealed the important role of miRNAs in mouse models of asthma ( 12 ). miR-106b-5p has been associated with glioma tumorigenesis ( 13 ), lung cancer ( 14 ), chronic myeloid leukemia ( 15 ), breast cancer ( 16 , 17 ) and hepatocellular carcinoma ( 18 ). However, the molecular mechanisms of miR-106b-5p in asthma remain unclear.…”

Section: Introductionmentioning

confidence: 99%

miR‑106b‑5p targeting SIX1 inhibits TGF‑β1‑induced pulmonary fibrosis and epithelial‑mesenchymal transition in asthma through regulation of E2F1

et al. 2021

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Asthma is an inflammatory disease of the airways, characterized by lung eosinophilia, mucus hypersecretion by goblet cells and airway hyper-responsiveness to inhaled allergens. The present study aimed to identify the function of microRNA (miR/miRNA)-106b-5p in TGF-β1-induced pulmonary fibrosis and epithelial-mesenchymal transition (EMT) via targeting sine oculis homeobox homolog 1 (SIX1) through regulation of E2F transcription factor 1 (E2F1) in asthma. Asthmatic mouse models were induced with ovalbumin. miRNA expression was evaluated using reverse transcription-quantitative PCR. Transfection experiments using bronchial epithelial cells were performed to determine the target genes. A luciferase reporter assay system was applied to identify the target gene of miR-106b-5p. The present study revealed downregulated miR-106b-5p expression and upregulated SIX1 expression in asthmatic mice and TGF-β1-induced BEAS-2B cells. Moreover, miR-106b-5p overexpression inhibited TGF-β1-induced fibrosis and EMT in BEAS-2B cells, while miR-106b-5p-knockdown produced the opposite effects. Subsequently, miR-106b-5p was found to regulate SIX1 through indirect regulation of E2F1. Additionally, E2F1- and SIX1-knockdown blocked TGF-β1-induced fibrosis and EMT in BEAS-2B cells. In addition, miR-106b-5p negatively regulated SIX1 via E2F1 in BEAS-2B cells. The present study demonstrated that the miR-106b-5p/E2F1/SIX1 signaling pathway may provide potential therapeutic targets for asthma.

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miR‐106b‐5p promotes aggressive progression of hepatocellular carcinoma via targeting RUNX3

Cited by 31 publications

References 31 publications

Identification of miRNA Master Regulators in Breast Cancer

Identification of miRNA Master Regulators in Breast Cancer

MiR-106b-5p regulates the migration and invasion of colorectal cancer cells by targeting FAT4

miR‑106b‑5p targeting SIX1 inhibits TGF‑β1‑induced pulmonary fibrosis and epithelial‑mesenchymal transition in asthma through regulation of E2F1

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