miR-548b-3p Regulates Proliferation, Apoptosis, and Mitochondrial Function by Targeting CIP2A in Hepatocellular Carcinoma

Lin, Lin; Wang, Yong

doi:10.1155/2018/7385426

Cited by 10 publications

(10 citation statements)

References 23 publications

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“…46,47 Data from previous investigations reveal that upregulation of miR-548b reduced the growth and metastatic behaviors of cancer cells. 26,48 Yun et al have demonstrated that miRNA-548b reduces the invasive behaviors of HCC by modulating HMGB1. 24 Lin et al performed an in vitro experiment of HCC cells and provided evidence that HCC cell growth and apoptosis are regulated by miR-548b.…”

Section: Discussionmentioning

confidence: 99%

“…24 Lin et al performed an in vitro experiment of HCC cells and provided evidence that HCC cell growth and apoptosis are regulated by miR-548b. 48 Meanwhile, miR- 198 FENG 548-3p is markedly downregulated in breast cancer and overexpression of miR-548-3p inhibits proliferation and promotes the apoptosis of breast cancer cells. 49 The author's in vitro experiments also indicated that miR-548b decreased the cell viability and colony-forming ability of melanoma cells, while transfection of miR-548b inhibitor caused completely opposite results.…”

Section: Discussionmentioning

confidence: 99%

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miR-548b Suppresses Melanoma Cell Growth, Migration, and Invasion by Negatively Regulating Its Target Gene HMGB1

Feng

2021

Cancer Biotherapy and Radiopharmaceuticals

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Background: Melanoma is one of the most aggressive malignancies. Exploration of metastasis-related genes will improve the clinical outcomes of patients with melanoma. Recently, microRNAs (miRNAs) have been implicated in regulating the aggressiveness of melanoma. In the current study, the author demonstrated the expression of miR-548b and its functions in melanoma. Materials and Methods: The expression levels of miR-548b and high mobility group protein 1 (HMGB1) in melanoma specimens and adjacent normal tissues were examined using the quantitative real-time PCR method. The Cell Counting Kit-8 (CCK-8), wound healing test, and Transwell assays were conducted to examine the impact of miR-548b on aggressive phenotypes of melanoma cells. The protein expression of HMGB1 was detected by Western blot. The tumor growth of melanoma cells in vivo was analyzed using the transplanted tumor model. The expression of HMGB1 in vivo was assessed using immunohistochemistry assay. Results: miR-548b was significantly downregulated in the melanoma sample when compared with adjacent normal tissues. In addition, low levels of miR-548b were related to poor overall survival in patients with melanoma. As predicted, overexpression of miR-548b suppressed the growth and metastasis-associated traits of melanoma cells. Furthermore, the luciferase reporter gene assay and Western blotting revealed that HMGB1 was a target of miR-548b and its expression level was negatively modulated by miR-548b. Several rescue experiments indicated that reintroduction of HMGB1 abolished the inhibiting effects of miR-548b on melanoma cells. Finally, the author demonstrated that upregulation of miR-548b repressed melanoma cell growth in vivo. Conclusions: All these findings demonstrate that miR-548b serves as a cancer-suppressive miRNA in human melanoma by inhibiting HMGB1.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

miR-548b Suppresses Melanoma Cell Growth, Migration, and Invasion by Negatively Regulating Its Target Gene HMGB1

Feng

2021

Cancer Biotherapy and Radiopharmaceuticals

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“… 64 miR‐548b‐3p and miR‐326 are tumor suppressors in adult HCC and other cancers although their role in FLC remains to be determined. 65 , 66 , 67 , 68 , 69 , 70 , 71 , 72 , 73 , 74 , 75 , 76 , 77 , 78 Ontology analysis of upregulated target mRNAs of top‐ranked downregulated miRNAs indicates activation of processes reported to be altered in FLC including those involved in extracellular matrix, integrin signaling, response to hypoxia, and inflammatory response in addition to signaling pathways involved in oncogenesis and fibrosis (Figure 2 ). 79 , 80 , 81 , 82 Analysis of downregulated target mRNAs of top‐ranked upregulated miRNAs indicated that downregulated processes were those related to normal liver functions including lipid metabolism, bile acid metabolism, drug metabolism, oxidation–reduction process, and coagulation cascades.…”

Section: Resultsmentioning

confidence: 99%

Integrated analysis using ToppMiR uncovers altered miRNA– mRNA regulatory networks in pediatric hepatocellular carcinoma—A pilot study

et al. 2022

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Background Pediatric hepatocellular carcinoma (HCC) is a group of liver cancers whose mechanisms behind their pathogenesis and progression are poorly understood. Aim We aimed to identify alterations in the expression of miRNAs and their putative target mRNAs in not only tumor tissues of patients with pediatric HCC but also in corresponding non‐tumorous background livers by using liver tissues without underlying liver disease as a control. Methods and results We performed a small‐scale miRNA and mRNA profiling of pediatric HCC (consisting of fibrolamellar carcinoma [FLC] and non‐FLC HCC) and paired liver tissues to identify miRNAs whose expression levels differed significantly from control livers without underlying liver disease. ToppMiR was used to prioritize both miRNAs and their putative target mRNAs in a gene‐annotation network, and the mRNA profile was used to refine the prioritization. Our analysis generated prioritized lists of miRNAs and mRNAs from the following three sets of analyses: (a) pediatric HCC versus control; (b) FLC versus control; and (c) corresponding non‐tumorous background liver tissues from the same patients with pediatric HCC versus control. No liver disease liver tissues were used as the control group for all analyses. Many miRNAs whose expressions were deregulated in pediatric HCC were consistent with their roles in adult HCC and/or other non‐hepatic cancers. Our gene ontology analysis of target mRNAs revealed enrichment of biological processes related to the sustenance and propagation of cancer and significant downregulation of metabolic processes. Conclusion Our pilot study indicates that alterations in miRNA–mRNA networks were detected in not only tumor tissues but also corresponding non‐tumorous liver tissues from patients with pediatric HCC, suggesting multi‐faceted roles of miRNAs in disease progression. Our results may lead to novel hypotheses for future large‐scale studies.

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“…Among them, the miR-548 family, with over 80 identified miRNAs, regulates the immune process in some diseases, such as cancer ( 88 , 89 ). A large amount studies have shown that miRNA-548 suppresses tumor proliferate by binding WNT2 ( 90 ), murine double minute 2 ( 91 ), metastasis tumor-associated protein-2 ( 92 ), specificity protein 1 ( 93 ), cancerous inhibitor of protein phosphatase 2A ( 94 ), HMGB1 ( 95 ), and so on. Inhibiting or down-regulating miR-548 promotes the tumor proliferation ( 96 ).…”

Section: Discussionmentioning

confidence: 99%

Identification of the Association Between Toll-Like Receptors and T-Cell Activation in Takayasu’s Arteritis

Tian

Huang

et al. 2022

Front. Immunol.

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To explore the relationships between Toll-like receptors (TLRs) and the activation and differentiation of T-cells in Takayasu’s arteritis (TAK), using real-time fluorescence quantitative polymerase chain reaction, mRNA abundance of 29 target genes in peripheral blood mononuclear cells (PBMCs) were detected from 27 TAK patients and 10 healthy controls. Compared with the healthy control group, the untreated TAK group and the treated TAK group had an increased mRNA level of TLR2 and TLR4. A sample-to-sample matrix revealed that 80% of healthy controls could be separated from the TAK patients. Correlation analysis showed that the inactive-treated TAK group exhibited a unique pattern of inverse correlations between the TLRs gene clusters (including TLR1/2/4/6/8, BCL6, TIGIT, NR4A1, etc) and the gene cluster associated with T-cell activation and differentiation (including TCR, CD28, T-bet, GATA3, FOXP3, CCL5, etc). The dynamic gene co-expression network indicated the TAK groups had more active communication between TLRs and T-cell activation than healthy controls. BCL6, CCL5, FOXP3, GATA3, CD28, T-bet, TIGIT, IκBα, and NR4A1 were likely to have a close functional relation with TLRs at the inactive stage. The co-expression of TLR4 and TLR6 could serve as a biomarker of disease activity in treated TAK (the area under curve/sensitivity/specificity, 0.919/100%/90.9%). The largest gene co-expression cluster of the inactive-treated TAK group was associated with TLR signaling pathways, while the largest gene co-expression cluster of the active-treated TAK group was associated with the activation and differentiation of T-cells. The miRNA sequencing of the plasma exosomes combining miRDB, DIANA-TarBase, and miRTarBase databases suggested that the miR-548 family miR-584, miR-3613, and miR-335 might play an important role in the cross-talk between TLRs and T-cells at the inactive stage. This study found a novel relation between TLRs and T-cell in the pathogenesis of autoimmune diseases, proposed a new concept of TLR-co-expression signature which might distinguish different disease activity of TAK, and highlighted the miRNA of exosomes in TLR signaling pathway in TAK.

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miR-548b-3p Regulates Proliferation, Apoptosis, and Mitochondrial Function by Targeting CIP2A in Hepatocellular Carcinoma

Cited by 10 publications

References 23 publications

miR-548b Suppresses Melanoma Cell Growth, Migration, and Invasion by Negatively Regulating Its Target Gene HMGB1

miR-548b Suppresses Melanoma Cell Growth, Migration, and Invasion by Negatively Regulating Its Target Gene HMGB1

Integrated analysis using ToppMiR uncovers altered miRNA– mRNA regulatory networks in pediatric hepatocellular carcinoma—A pilot study

Identification of the Association Between Toll-Like Receptors and T-Cell Activation in Takayasu’s Arteritis

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