Inhibition of hedgehog signalling attenuates <scp>UVB</scp>‐induced skin photoageing

Kim, Wanyeon; Kim, EunGi; Yang, Hee Jung; Kwon, Tai-Wan; Han, SeoYoung; Lee, Sung-Min; Youn, HyeSook; Jung, Youngmi; Kang, ChulHee; Youn, BuHyun

doi:10.1111/exd.12735

Cited by 21 publications

(12 citation statements)

References 54 publications

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“…The mRNA levels were determined by qRT-PCR following previous study 50 . Total RNA from cells or from xenografted tumor was isolated by TRIzol® (15596-026, Invitrogen, Carlsbad, CA, USA).…”

Section: Methodsmentioning

confidence: 99%

TRAF4 promotes lung cancer aggressiveness by modulating tumor microenvironment in normal fibroblasts

Kim

Lee

et al. 2017

Sci Rep

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Normal fibroblasts surrounding tumor cells play a crucial role in cancer progression through formation of the tumor microenvironment. Because factors secreted from normal fibroblasts can modulate the tumor microenvironment, it is necessary to identify key factors associated with regulation of secreted factors and to investigate the molecular mechanisms contributing to the tumor microenvironment formation process. In this study, we found that radiation induced the expression and K63-linkage poly-ubiquitination of TRAF4 in normal lung fibroblasts. The K63-linkage poly-ubiquitinated TRAF4 formed complexes with NOX2 or NOX4 by mediating phosphorylated p47-phox in normal lung fibroblasts. Moreover, we showed that TRAF4 stabilized NOX complexes by decreasing lysosomal degradation of NOX2 and NOX4 after irradiation. NOX complexes increased endosomal ROS levels that were permeable into cytoplasm, leading to NF-κB-mediated ICAM1 up-regulation. Soluble ICAM1 was subsequently secreted into conditioned media of radiation-activated normal lung fibroblasts. The conditioned media from irradiated normal fibroblasts enhanced proliferation and epithelial-mesenchymal transition of non-small cell lung cancer cells both in vitro and in vivo. These results demonstrate that TRAF4 in irradiated fibroblasts is positively associated with aggressiveness of adjacent cancer cells by altering the tumor microenvironment. Thus, we suggest that regulation of TRAF4 might be a promising strategy for cancer therapy.

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Section: Methodsmentioning

confidence: 99%

TRAF4 promotes lung cancer aggressiveness by modulating tumor microenvironment in normal fibroblasts

Kim

Lee

et al. 2017

Sci Rep

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“…26 Frozen patient tumor/normal lung tissues were fixed in formalin, dehydrated and embedded in paraffin blocks, which were then sectioned at 4 μm. The sections were subsequently incubated in 3% hydrogen peroxide/methanol and then in 0.25% pepsin (Dako, Carpinteria, CA, USA) to retrieve the antigens.…”

Section: Methodsmentioning

confidence: 99%

TFAP2C-mediated upregulation of TGFBR1 promotes lung tumorigenesis and epithelial–mesenchymal transition

Kim

Lee

et al. 2016

Exp Mol Med

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TFAP2C (transcription factor-activating enhancer-binding protein 2C) expression has been positively correlated with poor prognosis in patients with certain types of cancer, but the mechanisms underlying TFAP2C-mediated tumorigenesis in non-small-cell lung cancer (NSCLC) are still unknown. We previously performed a microarray analysis to identify TFAP2C regulation genes, and TGFBR1 (transforming growth factor-β receptor type 1) was found to be upregulated by TFAP2C. We observed that TFAP2C or TGFBR1 overexpression led to oncogenic properties, such as cell viability, proliferation and cell cycle progression. TGFBR1 upregulation induced by TFAP2C also promoted cell motility and migration, leading to malignant development. We also found that PAK1 (p21 protein (Cdc42/Rac)-activated kinase 1) signaling was involved in TFAP2C/TGFBR1-induced tumorigenesis. These results were confirmed by an in vivo xenograft model and patient tissue samples. This study shows that TFAP2C promoted tumor progression by upregulation of TGFBR1 and consequent activation of PAK1 signaling.

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“…Gene expression levels were assessed by real time qRT-PCR as described previously 47 48 with several modifications. Detailed procedure is demonstrated in Supplementary Materials and Methods .…”

Section: Methodsmentioning

confidence: 99%

Inhibitory effect of traditional oriental medicine-derived monoamine oxidase B inhibitor on radioresistance of non-small cell lung cancer

Son

Jun

Seo

et al. 2016

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Increased survival of cancer cells mediated by high levels of ionizing radiation (IR) reduces the effectiveness of radiation therapy for non-small cell lung cancer (NSCLC). In the present study, danshensu which is a selected component of traditional oriental medicine (TOM) compound was found to reduce the radioresistance of NSCLC by inhibiting the nuclear factor-κB (NF-κB) pathway. Of the various TOM compounds reported to inhibit the IR activation of NF-κB, danshensu was chosen as a final candidate based on the results of structural comparisons with human metabolites and monoamine oxidase B (MAOB) was identified as the putative target enzyme. Danshensu decreased the activation of NF-κB by inhibiting MAOB activity in A549 and NCI-H1299 NSCLC cells. Moreover, it suppressed IR-induced epithelial-to-mesenchymal transition, expressions of NF-κB-regulated prosurvival and proinflammatory genes, and in vivo radioresistance of mouse xenograft models. Taken together, this study shows that danshensu significantly reduces MAOB activity and attenuates NF-κB signaling to elicit the radiosensitization of NSCLC.

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Inhibition of hedgehog signalling attenuates UVB‐induced skin photoageing

Cited by 21 publications

References 54 publications

TRAF4 promotes lung cancer aggressiveness by modulating tumor microenvironment in normal fibroblasts

TRAF4 promotes lung cancer aggressiveness by modulating tumor microenvironment in normal fibroblasts

TFAP2C-mediated upregulation of TGFBR1 promotes lung tumorigenesis and epithelial–mesenchymal transition

Inhibitory effect of traditional oriental medicine-derived monoamine oxidase B inhibitor on radioresistance of non-small cell lung cancer

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