LARP6 Regulates Keloid Fibroblast Proliferation, Invasion, and Ability to Synthesize Collagen

Chen, Lingxi; Su, Yingjun; Yin, Bin; Li, Shu; Cheng, Xialin; He, Yan; Jia, Chiyu

doi:10.1016/j.jid.2022.01.028

Cited by 6 publications

(5 citation statements)

References 42 publications

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“…Blockade of this paracrine activin A-mDia2 axis suppresses cancer cell malignancy and squamous carcinogenesis in vitro and in vivo [ 86 , 87 ]. As for facilitated invasiveness, keloid tissue-derived fibroblasts (KF) with upregulated LARP6 expression demonstrates enhanced cell proliferation and invasive behavior in cell culture system, while knockdown of LARP reverses this effect, with reduced deposition of type I collagen and inhibition of proliferation and invasion ability [ 88 ]. In another study, Tan et al revealed the role of PPAR β / δ in the epithelial-mesenchymal communication involved in cellular redox homeostasis.…”

Section: Fibroblasts and Cancer-associated Fibroblastsmentioning

confidence: 99%

Fibroblasts in Scar Formation: Biology and Clinical Translation

Qian

Shan

Gong

et al. 2022

Oxidative Medicine and Cellular Longevity

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Scarring, which develops due to fibroblast activation and excessive extracellular matrix deposition, can cause physical, psychological, and cosmetic problems. Fibroblasts are the main type of connective tissue cells and play important roles in wound healing. However, the underlying mechanisms of fibroblast in reaching scarless wound healing require more exploration. Herein, we systematically reviewed how fibroblasts behave in response to skin injuries, as well as their functions in regeneration and scar formation. Several biocompatible materials, including hydrogels and nanoparticles, were also suggested. Moreover, factors that concern transformation from fibroblasts into cancer-associated fibroblasts are mentioned due to a tight association between scar formation and primary skin cancers. These findings will help us better understand skin fibrotic pathogenesis, as well as provide potential targets for scarless wound healing therapies.

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Section: Fibroblasts and Cancer-associated Fibroblastsmentioning

confidence: 99%

Fibroblasts in Scar Formation: Biology and Clinical Translation

Qian

Shan

Gong

et al. 2022

Oxidative Medicine and Cellular Longevity

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“…When we review the details of those proteins, they are all related to cancer development [8][9][10][11][12][13][14]. SFPQ [18][19][20], RTN4 [12,21], RICTOR [22][23][24][25][26], LARP6 [27][28][29][30], and HELLS [8][9][10]31,32] are all associated with cancer.…”

Section: Results 21 Sfpq Has Highest Expression In a Panel Of Overexp...mentioning

confidence: 99%

SFPQ and Its Isoform as Potential Biomarker for Non-Small-Cell Lung Cancer

Yang

Gilbertsen

Jacobson

et al. 2023

IJMS

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Cancer markers are measurable molecules in the blood or tissue that are produced by tumor cells or immune cells in response to cancer progression. They play an important role in clinical diagnosis, prognosis, and anti-drug monitoring. Although DNA, RNA, and even physical images have been used, proteins continue to be the most common marker. There are currently no specific markers for lung cancer. Metastatic lung cancer, particularly non-small-cell lung cancer (NSCLC), is one of the most common causes of death. SFPQ, YY1, RTN4, RICTOR, LARP6, and HELLS are expressed at higher levels in cells from NSCLC than in control or cells from inflammatory diseases. SFPQ shows the most difference between the three cell types. Furthermore, the cytoplasmic isoform of SFPQ is only found in advanced cancers. We have developed ELISAs to detect SFPQ and the long and short isoforms. Evidence has shown that the short isoform exists primarily in cancers. Furthermore, immunocytometry studies and IHC analysis have revealed that SFPQ levels are consistent with ELISA results. In addition, enhanced DNA methylation in the SFPQ gene may facilitate the SFPQ expression differences between control and cancer cells. Considering this, elevated SFPQ level and the isoform location could serve as a cancer diagnostic and prognostic marker.

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“…The loss of function or abnormal expression of RNA-binding proteins (RBP) will affect the AS changes and then affect the proliferation and metastasis of cancer cells. The current study on keloid found that RBP LARP6 can regulate collagen synthesis in fibroblasts and promote the proliferation and invasion of tumor cells, thus enabling the rapid growth and invasion of fibroblasts in keloid lesions ( Chen et al, 2022 ). RBP FXR1 can also directly bind to circRNAs, thereby reducing fibroblast proliferation and extracellular matrix accumulation and increasing the level of apoptosis ( Wang et al, 2021 ).…”

Section: Introductionmentioning

confidence: 93%

Genome-wide analysis of dysregulated RNA-binding proteins and alternative splicing genes in keloid

Zhang

et al. 2023

Front. Genet.

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Introduction: The pathogenesis of keloids remains unclear.Methods: In this study, we analyzed RNA-Seq data (GSE113619) of the local skin tissue of 8 keloid-prone individuals (KPI) and 6 healthy controls (HC) before and 42 days after trauma from the gene expression omnibus (GEO) database. The differential alternative splicing (AS) events associated with trauma healing between KPIs and HCs were identifified, and their functional differences were analyzed by gene ontology (GO) and kyoto encyclopedia of genes and genomes (KEGG) pathways. The co-expression relationship of differentially alternative splicing genes and differentially expressed RNA binding proteins (RBPs) was established subsequently.Results: A total of 674 differential AS events between the KD42 and the KD0 and 378 differential AS events between the HD42 and the HD0 were discovered. Notably, most of the differential genes related to keloids are enriched in actin, microtubule cells, and cortical actin cytoskeletal tissue pathway. We observed a signifificant association between AS genes (EPB41, TPM1, NF2, PARD3) and trauma healing in KPIs and HCs. We also found that the differential expression of healthy controls-specifific trauma healing-related RBPs (TKT, FDPS, SAMHD1) may affect the response of HCs to trauma healing by regulating the AS of downstream trauma healing-related genes such as DCN and DST. In contrast, KPIs also has specifific differential expression of trauma healing related RBPs (S100A9, HspB1, LIMA1, FBL), which may affect the healing response of KPIs to trauma by regulating the AS of downstream trauma healing-related genes such as FN1 and TPM1.Discussion: Our results were innovative in revealing early wound healing-related genes (EPB41, TPM1, NF2, PARD3) in KPI from the perspective of AS regulated by RBPs.

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LARP6 Regulates Keloid Fibroblast Proliferation, Invasion, and Ability to Synthesize Collagen

Cited by 6 publications

References 42 publications

Fibroblasts in Scar Formation: Biology and Clinical Translation

Fibroblasts in Scar Formation: Biology and Clinical Translation

SFPQ and Its Isoform as Potential Biomarker for Non-Small-Cell Lung Cancer

Genome-wide analysis of dysregulated RNA-binding proteins and alternative splicing genes in keloid

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