We have previously observed that preirradiation with naturally occurring doses of near-infrared (IR) protects normal human dermal fibroblasts from ultraviolet (UV) cytotoxicity in vitro. This effect was observed in temperature-controlled conditions, without heat shock protein (Hsp72-70) induction. Moreover, IR inhibited UVB-induced apoptosis by modulating the Bcl2/Bax balance, pointing to a role of p53. Here, we show for the first time that p53-deficient SaOs cells are not protected from UVB cytotoxicity by IR preirradiation, suggesting that the response to IR is p53-dependent. Thus, we investigated the effect of IR on the p53 signaling pathway. Normal human dermal fibroblasts exposed in vitro to IR accumulated p53 protein, involving p53 stabilization and phosphorylation of serine 15 (Ser15) and Ser20. IR-induced p53 accumulation correlated with increased expression of p21 and GADD45, showing that IR also stimulates p53 transcriptional activity. By modulating UVB-induced targets of the p53 signaling pathway, IR irradiation appears to anticipate the UVB response and to prepare cells to better resist subsequent UV-induced stress. This is reinforced by the fact that IR preirradiation reduces the formation of UVB-induced thymine dimers.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1111/j.1600-0625.2005.00397.x | DOI Listing |
Cell Mol Life Sci
January 2025
Institute of Endotypes in Oncology, Metabolism, and Immunology, National Research Council, Via Pietro Castellino 111, Naples, Italy.
Breast cancer represents the primary cause of death of women under 65 in developed countries, due to the acquisition of multiple drug resistance mechanisms. The PI3K/AKT pathway is one of the major regulating mechanisms altered during the development of endocrine resistance and inhibition of steps in this signalling pathway are adopted as a key strategy to overcome this issue. ADP-ribosylation is a post-translational modification catalysed by PARP enzymes that regulates essential cellular processes, often altered in diseases.
View Article and Find Full Text PDFCell Death Dis
January 2025
Department of Clinical and Laboratory Sciences and Medical Biotechnology, National Taiwan University College of Medicine, Taipei, Taiwan.
The spatial role of M1 and M2 tumor-associated macrophages (M1/M2 TAMs) in precision medicine remains unclear. EGFR and TP53 are among the most frequently mutated genes in lung adenocarcinoma. We characterized the mutation status and density of M1/M2 TAMs within tumor islets and stroma in 117 lung adenocarcinomas using next-generation sequencing and immunohistochemistry, respectively.
View Article and Find Full Text PDFNat Commun
January 2025
Oncology Research & Development, Pfizer Inc., San Diego, CA, USA.
To better understand drug resistance mechanisms to CDK4/6 inhibitors and inform precision medicine, we analyze real-world multi-omics data from 400 HR+/HER2- metastatic breast cancer patients treated with CDK4/6 inhibitors plus endocrine therapies, including 200 pre-treatment and 227 post-progression samples. The prevalences of ESR1 and RB1 alterations significantly increase in post-progression samples. Integrative clustering analysis identifies three subgroups harboring different resistance mechanisms: ER driven, ER co-driven and ER independent.
View Article and Find Full Text PDFCell Signal
January 2025
Hepatic Surgery Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Clinical Medicine Research Center for Hepatic Surgery of Hubei Province, Key Laboratory of Organ Transplantation, Ministry of Education, NHC Key Laboratory of Organ Transplantation, Key Laboratory of Organ Transplantation, Chinese Academy of Medical Sciences, Wuhan, Hubei 430030, PR China. Electronic address:
The ribosomal protein L6 (RPL6) is significant in the progression of different cancer types. However, its precise role in hepatocellular carcinoma (HCC) remains unclear. This research demonstrated that the expression levels of RPL6 are notably decreased in HCC tissues.
View Article and Find Full Text PDFFuture Sci OA
December 2025
Department of Gerontology, the First Affiliated Hospital, China Medical University, Shenyang, China.
Aim: The primary objective of this study is to investigate the impact of tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and its functional receptor, fibroblast growth factor-inducible 14 (Fn14), on the process of vascular smooth muscle cell (VSMC) senescence.
Methods: Rat arterial VSMCs were cultured with angiotensin II to establish a model of premature senescence. The effects of TWEAK and Fn14 on senescent VSMCs were evaluated.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!