MicroRNA‐329 upregulation impairs the HMGB2/β‐catenin pathway and regulates cell biological behaviors in melanoma

Mo, You; Fang, Ruihua; Wu, Jinhua; Su, Yuan; Jia, Shuqing; Li, Qun; Bai, Jingzhu; She, Xi‐Ning; Wang, Jianqin

doi:10.1002/jcp.28920

Cited by 27 publications

(23 citation statements)

References 46 publications

(69 reference statements)

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“…cdh1 (E-cadherin) is a core component of adherens junctions along with a-catenin and 1-catenin 23 . Interestingly, HMGB2 and 1-catenin have been reported to cooperate to promote melanoma progression 24 . These data demonstrate one of likely many signaling interactions that occur between interface cells and other cells adjacent to the tumor.…”

Section: Resultsmentioning

confidence: 99%

Spatially resolved transcriptomics reveals the architecture of the tumor/microenvironment interface

Hunter

Moncada²,

Weiss

et al. 2020

Preprint

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During tumor progression, cancer cells come into contact with new cell types in the microenvironment, but it is unclear how tumor cells adapt to new environments. Here, we integrate spatial transcriptomics and scRNA-seq to characterize tumor/microenvironment interactions during the initial steps of invasion. Using a zebrafish model of melanoma, we identify a unique "interface" cell state at the tumor/microenvironment boundary. This interface is composed of specialized tumor and microenvironment cells that upregulate a common set of cilia genes, and cilia proteins are enriched only where the tumor contacts the microenvironment. Cilia gene expression is regulated by ETS-family transcription factors, which normally act to suppress cilia genes outside of the interface. An ETS-driven interface is conserved across ten patient samples, suggesting it is a conserved feature of human melanoma. Our results demonstrate the power of spatial transcriptomic approaches in uncovering mechanisms that allow tumors to invade into the microenvironment.

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Section: Resultsmentioning

confidence: 99%

Spatially resolved transcriptomics reveals the architecture of the tumor/microenvironment interface

Hunter

Moncada²,

Weiss

et al. 2020

Preprint

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“…Zhang, Lu, and Gao (2019) identified that HMGB2 promoted proliferation of cervical cancer cells by activating AKT pathway. HMGB2 has also been proved to be involved in the regulation of the melanoma cell proliferation by inactivating the β‐catenin signaling pathway (Mo et al, 2019). Hence it is speculated that HMGB2 regulates cell proliferation through diverse mechanisms in different diseases.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‐127‐5p impairs function of granulosa cells via HMGB2 gene in premature ovarian insufficiency

Zhang

Dang

Liu

et al. 2020

Journal Cellular Physiology

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Distinct microRNA (miRNA) profiles have been reported in premature ovarian insufficiency (POI), but their functional relevance in POI is not yet clearly stated. In this study, aberrant expressions of miR‐127‐5p and high mobility group box 2 (HMGB2) were observed by microarrays in granulosa cells (GCs) from biochemical POI (bPOI) women and further confirmed by a quantitative reverse‐transcription polymerase chain reaction. Immortalized human granulosa cell line and mouse primary ovarian GCs were used for functional validation. Orthotopic mouse model was established to examine the role of miR‐127‐5p in vivo. Finally, the expression of miR‐127‐5p was measured in the plasma of bPOI women. The receiver operating characteristic curve analysis was performed to determine the indicative role of miR‐127‐5p for ovarian reserve. Results showed the upregulation of miR‐127‐5p was identified in GCs from bPOI patients. It inhibited GCs proliferation and impaired DNA damage repair capacity through targeting HMGB2, which was significantly downregulated in GCs from the same cohort of cases. miR‐127‐5p was confirmed to attenuate DNA repair capability via HMGB2 in mouse ovary in vivo. Intriguingly, the upexpression of miR‐127‐5p was also detected in plasma of bPOI individuals, suggesting that miR‐127‐5p could be a promising indicator for bPOI. Taken together, our results discovered the deleterious effects of miR‐127‐5p on GCs function and its predictive value in POI process. The target gene HMGB2 could be considered as a new candidate for POI. This study highlights the importance of DNA repair capacity for ovarian function and sheds light on the epigenetic mechanism in the pathogenicity of POI.

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“…In the present study, we demonstrated that knockdown of ADAM10 could inhibit the E-cadherin/β-catenin signaling pathway. Furthermore, β-catenin could regulate its target genes including MMP-9, Cyclin D1, c-Myc, and Survivin [33][34][35][36]. Knockdown of ADAM10 decreased the levels of those target genes, also indicating that ADAM10 could regulate E-cadherin/β-catenin signaling pathway.…”

Section: Discussionmentioning

confidence: 97%

ADAM10 promotes cell growth, migration, and invasion in osteosarcoma via regulating E-cadherin/β-catenin signaling pathway and is regulated by miR-122-5p

Yuan

Chen

et al. 2020

Cancer Cell Int

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Background: Osteosarcoma is a malignant bone tumor. Increasing evidences have revealed that a disintegrin and metalloproteinase 10 (ADAM10) is implicated in tumor development. The main purpose of this study is to explore the effects of ADAM10 on osteosarcoma cell functions and the underlying molecular mechanisms. Methods: Western blot and quantitative real-time PCR were performed to detect the expression of ADAM10 in one osteoblast (hFOB 1.19) and six osteosarcoma cells (Saos-2, SW1353, HOS, U-2OS, MG63, and 143B). The biological functions of ADAM10 in osteosarcoma cells were measured by cell counting kit-8 assay, flow cytometry, wound healing assay, and transwell assay. The interaction between miR-122-5p and ADAM10 was validated using dual-luciferase reporter assay. The effect of ADAM10 on the tumorigenicity of osteosarcoma cells was evaluated in a nude mice model in vivo. Results: We found that the expression of ADAM10 was relatively high in osteosarcoma cells compared with that in osteoblast. ADAM10 promoted osteosarcoma cell growth, migration, and invasion. Mechanism studies showed that knockdown of ADAM10 inactivated E-cadherin/β-catenin signaling pathway, as evidenced by increased the level of E-cadherin, reduced nuclear translocation of β-catenin, and decreased the levels of MMP-9, Cyclin D1, c-Myc, and Survivin. Downregulation of ADAM10 suppressed the tumorigenicity of osteosarcoma cells in vivo. Furthermore, ADAM10 was validated to be a downstream target of microRNA-122-5p (miR-122-5p). MiR-122-5p-induced inhibition of cell proliferation, migration, and invasion was reversed by overexpression of ADAM10 in osteosarcoma cells. Conclusions: Collectively, the key findings of this study are that ADAM10 promotes osteosarcoma cell proliferation, migration, and invasion by regulating E-cadherin/β-catenin signaling pathway, and miR-122-5p can target ADAM10, indicating that miR-122-5p/ADAM10 axis might serve as a therapeutic target of osteosarcoma.

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MicroRNA‐329 upregulation impairs the HMGB2/β‐catenin pathway and regulates cell biological behaviors in melanoma

Cited by 27 publications

References 46 publications

Spatially resolved transcriptomics reveals the architecture of the tumor/microenvironment interface

Spatially resolved transcriptomics reveals the architecture of the tumor/microenvironment interface

MicroRNA‐127‐5p impairs function of granulosa cells via HMGB2 gene in premature ovarian insufficiency

ADAM10 promotes cell growth, migration, and invasion in osteosarcoma via regulating E-cadherin/β-catenin signaling pathway and is regulated by miR-122-5p

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