ADAM17 regulates the proliferation and extracellular matrix of keloid fibroblasts by mediating the EGFR/ERK signaling pathway

Xin, Le; Fan, Youfen

doi:10.1080/2000656x.2021.2017944

Cited by 6 publications

(6 citation statements)

References 36 publications

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“…In addition to post-translational modifications, ADAM17 also affects post-transcriptional regulation. ADAM17 is highly expressed or upregulated in cancer (76,77) and other inflammation-related diseases, including kidney disease (78), sepsis (79), cicatrization (80), diabetic retinopathy (81), myocardial fibrosis (82), aortic dissection (83), arthritis (84) and atherosclerosis (7). The guanine-cytosine (G-C) sequences in the promoter region of ADAM17 are capable of binding specifically to many transcription factors (85)(86)(87).…”

Section: Adam17 Affects Post-transcriptional Regulationmentioning

confidence: 99%

Immunomodulatory role of metalloproteinase ADAM17 in tumor development

et al. 2022

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ADAM17 is a member of the a disintegrin and metalloproteinase (ADAM) family of transmembrane proteases involved in the shedding of some cell membrane proteins and regulating various signaling pathways. More than 90 substrates are regulated by ADAM17, some of which are closely relevant to tumor formation and development. Besides, ADAM17 is also responsible for immune regulation and its substrate-mediated signal transduction. Recently, ADAM17 has been considered as a major target for the treatment of tumors and yet its immunomodulatory roles and mechanisms remain unclear. In this paper, we summarized the recent understanding of structure and several regulatory roles of ADAM17. Importantly, we highlighted the immunomodulatory roles of ADAM17 in tumor development, as well as small molecule inhibitors and monoclonal antibodies targeting ADAM17.

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Section: Adam17 Affects Post-transcriptional Regulationmentioning

confidence: 99%

Immunomodulatory role of metalloproteinase ADAM17 in tumor development

et al. 2022

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“…Activation of ADAM17 by carcinogenic forms of Src has been reported to help promote tumorigenesis by enhancing signaling via EGFR and ERK in an autocrine and paracrine manner ( 44 ). Silencing ADAM17 may repress the activity of the EGFR/ERK pathway to reduce the proliferation of keloid fibroblasts ( 45 ). Consistently, the experiments that were conducted in the present study revealed that HOXC10 enhanced ADAM17 expression, increased the ADAM17-activated EGFR-ERK pathway, and contributed to the proliferation of HNSCC.…”

Section: Discussionmentioning

confidence: 99%

m⁶A‑modified HOXC10 promotes HNSCC progression via co‑activation of ADAM17/EGFR and Wnt/β‑catenin signaling

Zhou,

Huang,

et al. 2023

Int J Oncol

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The homeobox (HOX) gene family plays a fundamental role in carcinogenesis. However, the oncogenic mechanism of HOXC10 in head and neck squamous cell carcinoma (HNSCC) remains unclear. In the present study, it was revealed that HOXC10 expression was significantly higher in HNSCC tissues than in adjacent tissues, and a high level of HOXC10 was closely associated with worse clinical outcomes. HOXC10 overexpression promoted HNSCC cell proliferation, migration, and invasion, both in vitro and in vivo . Mechanistically, chromatin immunoprecipitation sequencing revealed that HOXC10 drove the transcriptional activation of a disintegrin and metalloproteinase 17 (ADAM17), and the ADAM17/epidermal growth factor receptor (EGFR)/ERK1/2 signaling pathway facilitating the proliferation of HNSCC. Furthermore, mass spectrometric analysis indicated that HOXC10 interacted with ribosomal protein S15A (RPS15A) and enhanced RPS15A protein expression, activating the Wnt/β-catenin pathway and contributing to invasion and metastasis of HNSCC. Additionally, the methylated RNA immune precipitation and RNA antisense purification assays showed that N 6 -methyladenosine (m 6 A) writer, methyltransferase-like 3, catalyzed m 6 A modification of the HOXC10 transcript, m 6 A reader insulin like growth factor 2 mRNA binding protein (IGF2BP)1 and IGF2BP3 involved in recognizing and stabilizing m 6 A-tagged HOXC10 mRNA. In summary, the present study identified HOXC10 as a promising candidate oncogene in HNSCC. The m 6 A modification-mediated HOXC10 promoted proliferation, migration, and invasion of HNSCC through co-activation of ADAM17/EGFR and Wnt/β-catenin signaling, providing a novel diagnostic and prognostic biomarker and a potential therapeutic target for HNSCC.

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“…Based on this, LOX and LOX-like family members could be seen as potential therapeutic targets for skin fibrosis and keloid tissue formation (108). In addition, Le found that silencing metalloproteinase protein 17 (ADAM17) may limit ECM deposition in keloid fibroblasts by inhibiting the activity of the EGFR/ERK pathway, thereby reducing proliferation, invasion, and migration (109).…”

Section: Epidermal Growth Factormentioning

confidence: 99%

Progress in the clinical treatment of keloids

Qi,

Xiao,

Tong

et al. 2023

Front. Med.

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Keloid is a pathological scar that is higher than the skin surface following skin damage. Its lesion range often extends beyond the original damage boundary and does not naturally subside over time. Its pathogenesis is very complex, currently the main causes include fibroblast excessive proliferation, collagen and extracellular matrix (Extracellular matrix, ECM) excessive deposition, excessive angiogenesis, and so on. The traditional treatment method primarily involves surgical intervention, but it is associated with a high recurrence rate post-surgery. Consequently, many treatment methods are derived according to the different clinical characteristics of keloid. This paper will review the therapeutic progress in recent years from surgical treatment, physiotherapy, drug therapy, and biological therapy, with the goal of offering valuable insights for the clinical treatment of keloids.

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ADAM17 regulates the proliferation and extracellular matrix of keloid fibroblasts by mediating the EGFR/ERK signaling pathway

Cited by 6 publications

References 36 publications

Immunomodulatory role of metalloproteinase ADAM17 in tumor development

Immunomodulatory role of metalloproteinase ADAM17 in tumor development

m⁶A‑modified HOXC10 promotes HNSCC progression via co‑activation of ADAM17/EGFR and Wnt/β‑catenin signaling

Progress in the clinical treatment of keloids

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ADAM17 regulates the proliferation and extracellular matrix of keloid fibroblasts by mediating the EGFR/ERK signaling pathway

Cited by 6 publications

References 36 publications

Immunomodulatory role of metalloproteinase ADAM17 in tumor development

Immunomodulatory role of metalloproteinase ADAM17 in tumor development

m6A‑modified HOXC10 promotes HNSCC progression via co‑activation of ADAM17/EGFR and Wnt/β‑catenin signaling

Progress in the clinical treatment of keloids

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m⁶A‑modified HOXC10 promotes HNSCC progression via co‑activation of ADAM17/EGFR and Wnt/β‑catenin signaling