Fibromodulin overexpression drives oral squamous cell carcinoma via activating downstream EGFR signaling

Xia, Lingyun; Zhang, Tianshu; Yao, Juncheng; Lu, Kaitian; Hu, Ziqiu; Gu, Xinsheng; Chen, Yongji; Qin, Shanshan; Leng, Weidong

doi:10.1016/j.isci.2023.108201

iScience

2023

DOI: 10.1016/j.isci.2023.108201

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Fibromodulin overexpression drives oral squamous cell carcinoma via activating downstream EGFR signaling

Lingyun Xia,

Tianshu Zhang,

Juncheng Yao

et al.

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Cited by 6 publications

References 37 publications

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MiR‐494‐3p regulates skin fibroblast activities by mediating fibromodulin production

Zhao,

Wang,

Zhang

et al. 2024

Journal Cellular Physiology

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Skin wound healing is a well‐coordinated process in which various cells and factors participate, during which fibroblast exhibits a critical role by exerting its multiple activities, including proliferation, migration, invasion, and differentiation. Previous studies have identified that fibromodulin (FMOD) could enhance dermal wound healing by promoting skin fibroblast activities, but little is known about its upstream regulator. We occasionally found that FMOD expression was downregulated in skin fibroblast by transforming growth factor‐β1 treatment. It was hypothesized that microRNAs (miRNA) in skin fibroblast could downregulate FMOD production and blocking them would increase FMOD expression, as well as promote skin wound healing. Here, by utilizing combined analysis of miRNA microarray from the Gene Expression Omnibus database and miRNA targets prediction, we successfully identified a miRNA, termed miR‐494‐3p, could regulate FMOD production in human skin fibroblast (BJ fibroblast). The functional analysis revealed that miR‐494‐3p mimics could inhibit BJ fibroblast migration and invasion but not proliferation and differentiation, while miR‐494‐3p inhibition markedly promotes migration, invasion, and differentiation of BJ fibroblast. Moreover, we established FMOD overexpression (OE) and knockout BJ fibroblast. We found that FMOD OE could rescue the inhibitory effects of miR‐494‐3p mimics on the migration and invasion of BJ fibroblast. In contrast, the miR‐494‐3p inhibitor transfection could not enhance migration, invasion, and differentiation of FMOD KO BJ fibroblast. Together, our results suggest that miR‐494‐3p may be a potential target for skin wound management via regulating FMOD production.

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MiR‐494‐3p regulates skin fibroblast activities by mediating fibromodulin production

Zhao,

Wang,

Zhang

et al. 2024

Journal Cellular Physiology

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PRELP inhibits the progression of oral squamous cell carcinoma via inactivation of the NF-κB pathway

Sun,

Chai,

Wang

et al. 2024

Archives of Oral Biology

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Matrisomics: Beyond the extracellular matrix for unveiling tumor microenvironment

Hong,

Jin,

Choi

et al. 2024

Biochimica et Biophysica Acta (BBA) - Reviews on Cancer

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Fibromodulin overexpression drives oral squamous cell carcinoma via activating downstream EGFR signaling

Cited by 6 publications

References 37 publications

MiR‐494‐3p regulates skin fibroblast activities by mediating fibromodulin production

MiR‐494‐3p regulates skin fibroblast activities by mediating fibromodulin production

PRELP inhibits the progression of oral squamous cell carcinoma via inactivation of the NF-κB pathway

Matrisomics: Beyond the extracellular matrix for unveiling tumor microenvironment

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