<scp>FBXL6</scp> is dysregulated in keloids and promotes keloid fibroblast growth by inducing <scp>c‐Myc</scp> expression

Feng, Guangdong; Sun, Hui; Piao, Meishan

doi:10.1111/iwj.13847

Cited by 3 publications

(2 citation statements)

References 31 publications

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“…Normal scars (three women, mean 35.7 years; n = 8) and keloid tissues (11 women, mean 37.4 years; n = 20) were obtained during reconstructive surgery as indicated in our previous research, and the clinical information could be referred. 14 Informed and written consents were signed by all participants enrolled, and the whole study was approved by the Ethics Committee of the Wuxi Second People's Hospital. This study followed the Declaration of Helsinki, Ethical Principles for Medical Research Involving Human Subjects.…”

Section: Methodsmentioning

confidence: 99%

The deubiquitinating enzyme USP37 promotes keloid fibroblasts proliferation and collagen production by regulating the c‐Myc expression

Piao

Feng

2022

International Wound Journal

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Previous research testifies that c‐Myc may promote keloid fibroblast proliferation and collagen accumulation. Ubiquitin‐specific peptidase 37 (USP37)‐mediated deubiquitination and stabilisation of c‐Myc are vital for lung cancer proliferation, while the potential role of USP37 in keloid fibroblasts is not investigated. Elevated USP37, c‐Myc, and Collagen I content were detected in keloid tissue with RT‐PCR or ELISA assay. USP37 over‐expression plasmids or USP37 short hairpin RNAs (shRNAs) were transfected into keloid fibroblasts with Lipofectamine 3000 to decipher the role of USP37 in keloid fibroblasts. USP37 overexpression could promote the proliferation of keloid fibroblasts with increased c‐Myc and Collagen I expression. On the other hand, USP37 shRNAs inhibited the proliferation of keloid fibroblasts with diminished c‐Myc and Collagen I expression. It was worth noting that C‐Myc overexpression promoted the proliferation of keloid fibroblasts inhibited by USP37 shRNAs with increasing Collagen I expression. All of these results demonstrate that USP37 could regulate c‐Myc to promote the proliferation and collagen deposit of keloid fibroblasts, and USP37 could be targeted in future keloid therapy.

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Section: Methodsmentioning

confidence: 99%

The deubiquitinating enzyme USP37 promotes keloid fibroblasts proliferation and collagen production by regulating the c‐Myc expression

Piao

Feng

2022

International Wound Journal

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“…• MYC gene expressed increased in microarray analysis of patient skin (Chen et al, 2004) • c-MYC overpexpression promotes the proliferation of keloid fibroblasts (Feng et al, 2023;Piao and Feng, 2023) • MYC protein expression increased in patient samples (Hu et al, 2002; Developmental diseases…”

Section: Neurodegenerationmentioning

confidence: 99%

MYC: there is more to it than cancer

Zacarías-Fluck,

Soucek,

Whitfield

2024

Front. Cell Dev. Biol.

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MYC is a pleiotropic transcription factor involved in multiple cellular processes. While its mechanism of action and targets are not completely elucidated, it has a fundamental role in cellular proliferation, differentiation, metabolism, ribogenesis, and bone and vascular development. Over 4 decades of research and some 10,000 publications linking it to tumorigenesis (by searching PubMed for “MYC oncogene”) have led to MYC becoming a most-wanted target for the treatment of cancer, where many of MYC’s physiological functions become co-opted for tumour initiation and maintenance. In this context, an abundance of reviews describes strategies for potentially targeting MYC in the oncology field. However, its multiple roles in different aspects of cellular biology suggest that it may also play a role in many additional diseases, and other publications are indeed linking MYC to pathologies beyond cancer. Here, we review these physiological functions and the current literature linking MYC to non-oncological diseases. The intense efforts towards developing MYC inhibitors as a cancer therapy will potentially have huge implications for the treatment of other diseases. In addition, with a complementary approach, we discuss some diseases and conditions where MYC appears to play a protective role and hence its increased expression or activation could be therapeutic.

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FBXL6 is dysregulated in keloids and promotes keloid fibroblast growth by inducing c‐Myc expression

Feng

Sun

Piao

2022

International Wound Journal

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C‐MYC‐mediated keloid fibroblasts proliferation and collagen deposit may contribute to the development of keloids. F‐box and leucine‐rich repeat protein 6 (FBXL6) is reported to be involved in tumour progression, while the role of FBXL6 in keloid fibroblasts is not deciphered. Normal control skins, hypertrophic scars and keloid tissues were collected and prepared for FBXL6 detection. FBXL6 short hairpin RNAs (shRNAs) or FBXL6 over‐expression plasmids were transfected into keloid fibroblasts, and then c‐MYC plasmids were further transfected. Cell viability was assayed with a Cell‐Counting Kit‐8 kit. The relative expression of FBXL6, Cyclin A1, Cyclin D2, Cyclin E1 and Collagen I was detected with real‐time PCR and Western blot. Elevated FBXL6 expression could be observed in keloid tissues and hypertrophic scars. FBXL6 shRNAs transfection could inhibit the viability of keloid fibroblasts with diminished c‐MYC expression and down‐regulated Cyclin A1, Cyclin D2, Cyclin E1 and Collagen I expression. At the same time, overexpressed FBXL6 could promote the proliferation of keloid fibroblasts. Overexpression of c‐MYC could promote the proliferation of keloid fibroblasts reduced by FBXL6 shRNAs with up‐regulated Cyclin A1 and Collagen I expression. FBXL6 could promote the growth of keloid fibroblasts by inducing c‐MYC expression, which could be targeted in keloids treatment.

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FBXL6 is dysregulated in keloids and promotes keloid fibroblast growth by inducing c‐Myc expression

Cited by 3 publications

References 31 publications

The deubiquitinating enzyme USP37 promotes keloid fibroblasts proliferation and collagen production by regulating the c‐Myc expression

The deubiquitinating enzyme USP37 promotes keloid fibroblasts proliferation and collagen production by regulating the c‐Myc expression

MYC: there is more to it than cancer

FBXL6 is dysregulated in keloids and promotes keloid fibroblast growth by inducing c‐Myc expression

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