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

Feng, Xien

doi:10.1089/cbr.2019.3507

Cited by 7 publications

(6 citation statements)

References 45 publications

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“…Guo et al reported that miR-18a-5p induces proliferation and inhibited apoptosis of melanoma cells by targeting EPHA7 [22]. Fen et al showed that miR-548b inhibits the growth and metastasis of melanoma by negatively regulating HMGB1 [23]. Our results indicate that miR-495-3p targets KPNA2 in melanoma.…”

Section: Discussionsupporting

confidence: 59%

CREB1 regulates KPNA2 by inhibiting mir-495-3p transcription to control melanoma progression

Geng

Qiu

Gao

et al. 2022

BMC Mol and Cell Biol

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Background Melanoma is a common type of skin cancer, and its incidence is increasing gradually. Exploring melanoma pathogenesis helps to find new treatments. Objective We aimed to explore the potential molecular mechanisms by which CREB1 regulates melanoma. Methods TransmiR and ALGGEN were used to predict targets of CREB1 in the promoter of miR-495-3p or miR-495-3p and KPNA2, and a dual-luciferase reporter assay was performed to detect binding of CREB1 to these promoters. In addition, binding of CREB1 to the miR-495-3p promoter was confirmed by a ChIP assay. qRT‒PCR was carried out to detect mRNA levels of miR-495-3p, CREB1 and KPNA2. An EdU assay was conducted to detect cell viability. Transwell assays and flow cytometry were performed to assess cell migration and invasion and apoptosis, respectively. Moreover, factors associated with overall survival were analysed by using the Cox proportional hazards model. Results Our results show miR-495-3p to be significantly decreased in melanoma. Additionally, miR-495-3p overexpression inhibited melanoma cell viability. CREB1 targeted miR-495-3p, and CREB1 overexpression enhanced melanoma cell viability by inhibiting miR-495-3p transcription. Moreover, miR-495-3p targeted KPNA2, and CREB1 regulated KPNA2 by inhibiting miR-495-3p transcription to enhance melanoma cell viability. Conclusion CREB1 regulates KPNA2 by inhibiting miR-495-3p transcription to control melanoma progression. Our results indicate the molecular mechanism by which the CREB1/miR-495-3p/KPNA2 axis regulates melanoma progression.

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Section: Discussionsupporting

confidence: 59%

CREB1 regulates KPNA2 by inhibiting mir-495-3p transcription to control melanoma progression

Geng

Qiu

Gao

et al. 2022

BMC Mol and Cell Biol

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“…HMGB1 is a target of miR-548b, and its expression level is negatively regulated by miR-548b, while the reintroduction of HMGB1 abolishes the inhibiting effects of miR-548b on melanoma cells. All these findings demonstrated that miR-548b might act as a cancer-suppressive miRNA in human melanoma by inhibiting HMGB1, thus suggesting potential systemic and local usefulness [ 15 ]. On a side note, miRNAs have also been evaluated for their role in drug response modulation, in particular for dabrafenib.…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, miRNAs can affect HMGB1 gene expression, modulating cancer progression. HMGB1 is a direct target of miR-548b, and the expression level of this miRNA can suppress melanoma cells’ growth by targeting the HMGB1 pathway [ 15 ].…”

Section: Introductionmentioning

confidence: 99%

Role of HMGB1 in Cutaneous Melanoma: State of the Art

Pomi

Borgia

Custurone

et al. 2022

IJMS

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High-mobility Group Box 1 (HMGB1) is a nuclear protein that plays a key role in acute and chronic inflammation. It has already been studied in several diseases, among them melanoma. Indeed, HMGB1 is closely associated with cell survival and proliferation and may be directly involved in tumor cell metastasis development thanks to its ability to promote cell migration. This research aims to assess the role of this molecule in the pathogenesis of human melanoma and its potential therapeutic role. The research has been conducted on the PubMed database, and the resulting articles are sorted by year of publication, showing an increasing interest in the last five years. The results showed that HMGB1 plays a crucial role in the pathogenesis of skin cancer, prognosis, and therapeutical response to therapy. Traditional therapies target this molecule indirectly, but future perspectives could include the development of new target therapy against HMGB1, thus adding a new approach to the therapy, which has often shown primary and secondary resistance. This could add a new therapy arm which has to be prolonged and specific for each patient.

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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 Suppresses Melanoma Cell Growth, Migration, and Invasion by Negatively Regulating Its Target Gene HMGB1

Cited by 7 publications

References 45 publications

CREB1 regulates KPNA2 by inhibiting mir-495-3p transcription to control melanoma progression

CREB1 regulates KPNA2 by inhibiting mir-495-3p transcription to control melanoma progression

Role of HMGB1 in Cutaneous Melanoma: State of the Art

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

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