miR-149* Suppresses Liver Cancer Progression by Down-Regulating Tumor Necrosis Factor Receptor 1–Associated Death Domain Protein Expression

Feng, Qingqing; Zhang, Hongli; Nie, Xiaobo; Li, Yuanqiang; Chen, Weidong; Wang, Yandong

doi:10.1016/j.ajpath.2019.10.010

Cited by 19 publications

(12 citation statements)

References 52 publications

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“…We recently showed that miR-206 is transferred by satellite cell EVs to fibrogenic cells during MOV to regulate collagen deposition, 7 and confirm here that miR-206 is the most abundant miRNA in MPC EVs ( Figure 2C ). Expanding on our earlier work, we found numerous miRNAs enriched in MPC EVs ( Figure 2C ) that are experimentally shown to lower Mmp9 expression, such as miR-24, 47–49 miR-149, 50–55 and miR-486, 56 , 57 as well as miRNAs that are validated to target the 3′-UTR of Mmp9 mRNA and reduce transcript levels, including Let-7e, 58 miR-133a and -133b, 59 , 60 and miR-320 61 ( Figure 2D ). In silico predicted miRNA-mRNA target analysis 62 further revealed that ECM remodeling is the most regulated process by MPC EV miRNAs ( Figure 2E , Tables S2 and S3 ).…”

Section: Resultssupporting

confidence: 68%

Fusion-Independent Satellite Cell Communication to Muscle Fibers During Load-Induced Hypertrophy

et al. 2020

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Abstract The “canonical” function of Pax7+ muscle stem cells (satellite cells) during hypertrophic growth of adult muscle fibers is myonuclear donation via fusion to support increased transcriptional output. In recent years, however, emerging evidence suggests that satellite cells play an important secretory role in promoting load-mediated growth. Utilizing genetically modified mouse models of delayed satellite cell fusion and in vivo extracellular vesicle tracking, we provide evidence for satellite cell communication to muscle fibers during hypertrophy. Myogenic progenitor cell extracellular vesicle-mediated communication to myotubes in vitro influences extracellular matrix (ECM)-related gene expression, which is congruent with in vivo overload experiments involving satellite cell depletion, as well as in silico analyses. Satellite cell-derived extracellular vesicles can transfer a Cre-induced, cytoplasmic-localized fluorescent reporter to muscle cells as well as miRNAs that regulate ECM genes such as matrix metalloproteinase 9 (Mmp9), which may facilitate growth. Delayed satellite cell fusion did not limit long-term load-induced muscle hypertrophy indicating that early fusion-independent communication from satellite cells to muscle fibers is an under-appreciated aspect of satellite cell biology. We cannot exclude the possibility that satellite cell-mediated myonuclear accretion is necessary to maintain prolonged growth, specifically in the later phases of adaptation, but these data collectively highlight how extracellular vesicle delivery from satellite cells can directly contribute to mechanical load-induced muscle fiber hypertrophy, independent of cell fusion to the fiber.

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Section: Resultssupporting

confidence: 68%

Fusion-Independent Satellite Cell Communication to Muscle Fibers During Load-Induced Hypertrophy

et al. 2020

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“…Hsa-mir-149 blocked paracrine interactions of macrophages via decreasing the expression of colony-stimulating factor-1 and epidermal growth factor, which could suppress breast cancer metastasis [31]. In liver cancer, mir-149 suppressed tumor progression by restraining the expression of tumor necrosis factor receptor type 1associated death domain protein in NF-κB signaling pathway [32]. Interestingly, in present study, higher expression of hsa-miR-149 meant worse prognosis in HCC.…”

Section: Discussionmentioning

confidence: 47%

Identification of 3-miRNA Signature for Predicting Prognosis in Patients with Hepatocellular Carcinoma

Qiu

Huang

et al. 2021

Preprint

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Background: Vascular invasion is closely related to the prognosis of hepatocellular carcinoma (HCC). Increasing evidence suggests that miRNAs can serve as biomarks to predict prognosis in various tumors. Thus, the aim of this study was to develop a novel, vascular invasion-related miRNA signature for prediction of HCC prognosis.Methods: Differentially expressed miRNAs (DEMs) between HCC samples with vascular invasion and without vascular invasion were obtained from GSE67140. MiRNAs expression profiles and clinical information for 344 patients were collected from The Cancer Genome Atlas database, and the patients were randomized (1:1) to training set and validation set. LASSO regression model was employed to identify survival-associated DEMs and establish risk score in the training set. Moreover, risk score was verified in the validation set. And nomogram based on risk score and clinical information was constructed to improve the prediction of prognosis. Meanwhile, four online tools were used to predict target genes and enrichment analysis was utilized to explore the biological pathway of the miRNAs.Results: A novel three-miRNA signature was screened including hsa-mir-210, hsa-mir-149 and hsa-mir-99a, and risk score was established for HCC prognosis prediction. Patients were divided into the low-risk group and high-risk group according to risk score. High-risk group both have higher hazard of death compared with low-risk group in training set and validation set. And the 5-year AUC of risk score were 0.718, 0.674 and 0.697 in training set, validation set and the total set, respectively. The C-index of nomogram was 0.724, and calibration curves showed nomogram had high concordance to predict 1- ,3- , and 5-year survival rates among HCC patients. Furthermore, enrichment analysis identified several tumor-associated pathways including Ras signaling pathway, PI3K-Akt signaling pathway, and MAPK signaling pathway and so on, which may contribute to explain the potential molecular mechanisms of above miRNAs.Conclusion: This study developed a risk assessment model based on three miRNAs, which could accurately predict the prognosis of HCC.

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“…miR-149 has been confirmed to play an important role in the occurrence and development of a variety of malignant tumors, and has the function of tumor suppressor gene. Feng et al using the miRNA gene chip technology to filtered may participate in regulating the liver metastasis of microRNAs, the results showed that the expression of miR-149 abnormal amount is reduced, at the same time the research by qRT-PCR method in patients with liver cancer and normal plasma, found that miR-149 expression in liver cancer patients plasma and tissue levels significantly lower than normal plasma and corresponding normal tissue adjacent to carcinoma [ 21 ]. Schaefer et al showed that the expression of miR-149 in prostate cancer tissues was significantly lower than that in corresponding adjacent normal tissues through miRNA microarray technology, and the results were verified by QRT PCR method to further confirm its authenticity [ 22 ].…”

Section: Discussionmentioning

confidence: 99%

LncRNA GACAT1 targeting miRNA-149 regulates the molecular mechanism of proliferation, apoptosis and autophagy of oral squamous cell carcinoma cells

Chen

et al. 2021

Aging

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To explore the effects of lncRNA GACAT1/miR-149 molecular axis on the proliferation, apoptosis, migration and autophagy of oral squamous cell carcinoma (OSCC) cells, and to explore its molecular mechanism. The expressions of lncRNA GACAT1 and miR-149 in tissues and cell lines of patients with OSCC were detected by qRT-PCR. Si-control, GACAT1-siRNA, inhibitor NC and miR-149 inhibitors were transfected into OSCC cells separately or in combination with Lipofectamine 2000. The binding sites between lncRNA GACAT1 and miR-149 were predicted using the miRanda website, and the targeting relationship was verified by dual-luciferase assay. The expression of lncRNA XIST and miR-149 was detected by qRT-PCR. CCK-8 assay was used to detect cell activity. Cell cycle distribution and apoptosis were detected by flow cytometry. Cell migration ability was detected by Transwell assay. The expression of migration and autophagy-related proteins was detected by western blot. LncRNA GACAT1 was highly expressed in cancer tissues and cell lines of OSCC patients ( P < 0.01), while miR-149 was low expressed ( P < 0.01). LncRNA GACAT1 binds to miR-149 targeting. The down-regulation of lncRNA GACAT1 inhibited the proliferation and migration of OSCC cells and promoted apoptosis and autophagy ( P < 0.01). The transfection of miR-149 inhibitor had the opposite effect. Knockdown of lncRNA GACAT1 and transfection with miR-149 inhibitor reversed the effect of GACAT1 silencing on OSCC cells. Inhibition of lncRNA GACAT1 can inhibit the proliferation and migration of OSCC cells, promote apoptosis and autophagy, and the mechanism may be related to the targeting of miR-149.

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miR-149* Suppresses Liver Cancer Progression by Down-Regulating Tumor Necrosis Factor Receptor 1–Associated Death Domain Protein Expression

Cited by 19 publications

References 52 publications

Fusion-Independent Satellite Cell Communication to Muscle Fibers During Load-Induced Hypertrophy

Fusion-Independent Satellite Cell Communication to Muscle Fibers During Load-Induced Hypertrophy

Identification of 3-miRNA Signature for Predicting Prognosis in Patients with Hepatocellular Carcinoma

LncRNA GACAT1 targeting miRNA-149 regulates the molecular mechanism of proliferation, apoptosis and autophagy of oral squamous cell carcinoma cells

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