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PI3K/AKT/mTOR Targeting in Colorectal Cancer Radiotherapy: A Systematic Review.
J Gastrointest Cancer
January 2025
Medical Physics Research Center, Basic Sciences Research Institute, Mashhad University of Medical Sciences, Mashhad, Iran.
Background: Radioresistance is a major challenge in the treatment of patients with colorectal cancer (CRC) and impairs the efficacy of radiotherapy. The PI3K/AKT/mTOR signaling pathway plays a critical role in CRC and contributes to the development of radioresistance. Accordingly, targeting this signaling pathway may be a promising strategy to improve oncotherapy.
View Article and Find Full Text PDFCellular senescence in the tumor with a bone niche microenvironment: friend or foe?
Clin Exp Med
January 2025
Department of Medical Genetics, School of Medicine, Tehran University of Medical Sciences (TUMS), Tehran, Iran.
Cellular senescence is understood to be a biological process that is defined as irreversible growth arrest and was originally recognized as a tumor-suppressive mechanism that prevents further propagation of damaged cells. More recently, cellular senescence has been shown to have a dual role in prevention and tumor promotion. Senescent cells carry a senescence-associated secretory phenotype (SASP), which is altered by secretory factors including pro-inflammatory cytokines, chemokines, and other proteases, leading to the alteration of the tissue microenvironment.
View Article and Find Full Text PDFMelatonin antagonizes bone loss induced by mechanical unloading via IGF2BP1-dependent mA regulation.
Cell Mol Life Sci
January 2025
The Key Laboratory of Aerospace Medicine, Ministry of Education, Air Force Medical University, Xi'an, 710032, Shaanxi, China.
Disuse bone loss is prone to occur in individuals who lack mechanical stimulation due to prolonged spaceflight or extended bed rest, rendering them susceptible to fractures and placing an enormous burden on social care; nevertheless, the underlying molecular mechanisms of bone loss caused by mechanical unloading have not been fully elucidated. Numerous studies have focused on the epigenetic regulation of disuse bone loss; yet limited research has been conducted on the impact of RNA modification bone formation in response to mechanical unloading conditions. In this study, we discovered that mA reader IGF2BP1 was downregulated in both osteoblasts treated with 2D clinostat and bone tissue in HLU mice.
View Article and Find Full Text PDFPharmacological and structural insights into nanvuranlat, a selective LAT1 (SLC7A5) inhibitor, and its N-acetyl metabolite with implications for cancer therapy.
Sci Rep
January 2025
Department of Bio-System Pharmacology, Graduate School of Medicine, Osaka University, 2-2, Yamadaoka, Suita, Osaka, 565-0871, Japan.
L-type amino acid transporter 1 (LAT1, SLC7A5), overexpressed in various cancers, mediates the uptake of essential amino acids crucial for tumor growth. It has emerged as a promising target for cancer therapy. Nanvuranlat (JPH203/KYT-0353), a LAT1 inhibitor, has shown antitumor activity in preclinical studies and efficacy in biliary tract cancer during clinical trials.
View Article and Find Full Text PDFLINC00626 drives tamoxifen resistance in breast cancer cells by interaction with UPF1.
Sci Rep
January 2025
The Second Department of Critical Care Medicine, The Second Affiliated Hospital of Anhui Medical University, Hefei, 230601, Anhui, China.
Although tamoxifen is commonly utilized as adjuvant therapy for Estrogen Receptor alpha (ERα)-positive breast cancer patients, approximately 30-50% of individuals treated with tamoxifen experience relapse. Therefore, it is essential to investigate additional factors besides ERα that influence the estrogen response. In this study, cross-analysis of databases were performed, and the results revealed a significant association between LINC00626 and ERα signaling as well as increased expression levels of this gene in tamoxifen-resistant cells.
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