AhR-E2F1-KGFR signaling is involved in KGF-induced intestinal epithelial cell proliferation

Yang, Kunqiu; Yin, Jiuheng; Sheng, Baifa; Han, Bin; Pu, Aimin; Yu, Min; Sun, Lihua; Xiao, Weidong; Yang, Hua

doi:10.3892/mmr.2017.6368

Cited by 8 publications

(6 citation statements)

References 30 publications

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“…In addition, in a previous study, the proliferation of epidermal cells was affected by KGF, epidermal growth factor, nerve growth factor, TGF, TNF-α and other cytokines (28). However, KGF is the most potent and specific cytokine that promotes keratinocyte proliferation (14,15,29). Therefore, the present study aimed to determine the effect of TGP on the KGF-induced hyperproliferation of HaCaT cells.…”

Section: Discussionmentioning

confidence: 88%

Inhibitory effects of TGP on KGF‑induced hyperproliferation of HaCaT cells via suppression of the p38 MAPK/NF‑κB p65 pathway

Pang

Cao

et al. 2018

Mol Med Report

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Psoriasis is a chronic inflammatory skin disease, primarily caused by overgrowth and abnormal differentiation of epidermal keratinocytes. Studies have suggested that keratinocyte growth factor (KGF) may be involved in the regulation of differentiation and development of keratinocytes. Total glucosides of peony (TGP) have been widely used for the treatment of psoriasis. The present study aimed to determine whether the therapeutic effect of TGP on psoriasis is mediated by modulation of the p38 mitogen‑activated protein kinase (p38 MAPK)/nuclear factor (NF)‑κB p65 signaling pathways. Cell proliferation was evaluated by CCK‑8 and cell cycle was assessed by flow cytometry assay. Protein and mRNA expression of genes were determined by western blot and reverse transcription‑quantitative polymerase chain reaction, respectively. The results of the present study demonstrated that KGF can promote proliferation of HaCaT cells in a dose‑dependent manner. In addition, it was demonstrated that TGP may suppress the hyperproliferation of HaCaT cells stimulated by KGF by inducing arrest of the cell cycle at the G1 phase. The expression levels of the proinflammatory cytokines interleukin (IL)‑22 and vascular endothelial growth factor (VEGF) were markedly elevated in cells treated with KGF, whereas they were downregulated in cells treated with TGP. Furthermore, combination treatments with p38 MAPK inhibitor SB203580 and KGF, or TGP and KGF suppressed the mRNA and protein expression levels of IL‑22 and VEGF, compared with cells treated with KGF alone. Furthermore, the expression profiles of phosphorylated‑p38 MAPK and NF‑κB p65 were similar to those of IL‑22 and VEGF. The results of the present study suggested that the therapeutic effect of TGP on psoriasis may be mediated by modulation of the p38 MAPK/NF‑κB p65 signaling pathway. The results of the present study contribute to the understanding of the role of TGP in the treatment of psoriasis. The present study provides insights suggesting that p38 MAPK may be a novel regulatory signaling pathway for the treatment of psoriasis.

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Section: Discussionmentioning

confidence: 88%

Inhibitory effects of TGP on KGF‑induced hyperproliferation of HaCaT cells via suppression of the p38 MAPK/NF‑κB p65 pathway

Pang

Cao

et al. 2018

Mol Med Report

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“…FGF7 also promoted healing of colonic anastomoses by increasing cell proliferation and mucus production and reducing inflammation [ 165 ]. Similarly, FGF7 attenuated I/R and radiation-induced injuries by reducing intestinal epithelial cell apoptosis and the disruption of tight junctions via an AhR–E2F1–FGFR2IIIb signaling pathway [ 166 , 167 ]. FGF7 and FGF10 promoted the repair of the resected small bowel via activating intestinal epithelial FGFR2IIIb [ 168 , 169 ].…”

Section: Reviewmentioning

confidence: 99%

Roles of the fibroblast growth factor signal transduction system in tissue injury repair

et al. 2022

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Following injury, tissue autonomously initiates a complex repair process, resulting in either partial recovery or regeneration of tissue architecture and function in most organisms. Both the repair and regeneration processes are highly coordinated by a hierarchy of interplay among signal transduction pathways initiated by different growth factors, cytokines and other signaling molecules under normal conditions. However, under chronic traumatic or pathological conditions, the reparative or regenerative process of most tissues in different organs can lose control to different extents, leading to random, incomplete or even flawed cell and tissue reconstitution and thus often partial restoration of the original structure and function, accompanied by the development of fibrosis, scarring or even pathogenesis that could cause organ failure and death of the organism. Ample evidence suggests that the various combinatorial fibroblast growth factor (FGF) and receptor signal transduction systems play prominent roles in injury repair and the remodeling of adult tissues in addition to embryonic development and regulation of metabolic homeostasis. In this review, we attempt to provide a brief update on our current understanding of the roles, the underlying mechanisms and clinical application of FGFs in tissue injury repair.

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“…The E5 oncoprotein of human papillomavirus type 16 (HPV16 E5) decreases KGFR/FGFR2b [45] resulting in the deregulation of signal transduction [46], and the induction of interferon regulatory factor 1 (IRF-1) stimulating interferin beta (IFN-b) [47]. One regulation of KGFR is by the transcription factor E2F1: knockout of activated aryl hydrocarbon receptor (AhR) led to KGFR downregulation and transfection with siRNA specific for AhR (siAhR) reduced E2F1 in the nucleus [48]. Thereby AhR-E2F1-KGFR signaling is actively involved in epithelial cell proliferation and early carcinogenesis.…”

Section: Keratinasementioning

confidence: 99%

Undervalued ubiquitous proteins

Brücher

Jamall

2019

4open

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The role of ubiquitous proteins (UPs) and their corresponding enzymes have been underestimated in carcinogenesis as the focus of much research revolved around measuring mutations and/or other genetic epiphenomena as surrogate markers of cancer and cancer progression. Over the past three decades, the scientific community has come to realize that the concentration on microdissection of cancer cells without accounting for the neighborhood in which these cells reside, i.e., the stroma, fails to reflect the true nature of cancer biology. UPs are fundamental for cellular homeostasis and phylogenetic development as well as for the integrity of the cytoskeleton and for the stability of cells and tissues in regards to intercellular signaling, cell shape and mobility, apoptosis, wound healing, and cell polarity. Corresponding enzymes are used by microorganisms to gain entry into the host by degradation of UPs and play a role to cleave peptide bonds for killing disease-causing life forms along for the creation of the precancerous niche (PCN) during carcinogenesis, cancer invasion, and in metastasis. The language used by such proteins as well as their complementary enzymes with its influence on multiple pathways and the cross-linked extracellular matrix is incompletely understood. The role of UPs in the disruption of signaling homeostasis and resulting interference with crosstalk in carcinogenesis appears sufficiently delineated to warrant a much more refined examination of their qualitative and quantitative contribution to the development of cancer and cancer therapy.

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AhR-E2F1-KGFR signaling is involved in KGF-induced intestinal epithelial cell proliferation

Cited by 8 publications

References 30 publications

Inhibitory effects of TGP on KGF‑induced hyperproliferation of HaCaT cells via suppression of the p38 MAPK/NF‑κB p65 pathway

Inhibitory effects of TGP on KGF‑induced hyperproliferation of HaCaT cells via suppression of the p38 MAPK/NF‑κB p65 pathway

Roles of the fibroblast growth factor signal transduction system in tissue injury repair

Undervalued ubiquitous proteins

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