Pyroptosis is a newly discovered programmed cell death mechanism involved in tumorigenesis. Long non-coding RNAs (lncRNAs) have been implicated in colorectal cancer (CRC). However, the potential role of pyroptosis-related lncRNAs (PRLs) in CRC remains unelucidated. Therefore, we retrieved transcriptomic data of CRC patients from The Cancer Genome Atlas (TCGA). With the use of univariate and multivariate Cox proportional hazards regression models and the random forest algorithm, a new risk model was constructed based on eight PRLs: , and . Then, according to the Kaplan-Meier plots, the relationship of PRLs with the survival of CRC patients was explored and validated with our risk model in external datasets (Gene Expression Omnibus (GEO) databases; GEO17536, n = 177, and GSE161158, n = 250). To improve its clinical utility, a nomogram combining PRLs that could predict the clinical outcome of CRC patients was established. A full-spectrum immune landscape of CRC patients mediated by PRLs could be described. The PRLs were stratified into two molecular subtypes involved in immune modulators, immune infiltration of tumor immune microenvironment, and inflammatory pathways. Afterward, Tumor Immune Dysfunction and Exclusion (TIDE) and microsatellite instability (MSI) scores were analyzed. Three independent methods were applied to predict PRL-related sensitivity to chemotherapeutic drugs. Our comprehensive analysis of PRLs in CRC patients demonstrates a potential role of PRLs in predicting response to treatment and prognosis of CRC patients, which may provide a better understanding of molecular mechanisms underlying CRC pathogenesis and facilitate the development of effective immunotherapy.
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http://dx.doi.org/10.3389/fonc.2022.983895 | DOI Listing |
Unlabelled: Dysregulated epigenetic programs that restrict differentiation, reactivate fetal genes, and confer phenotypic plasticity are critical to colorectal cancer (CRC) development. By screening a small molecule library targeting epigenetic regulators using our dual reporter system, we found that inhibiting histone deacetylase (HDAC) 1/2 promotes CRC differentiation and anti-tumor activity. Comprehensive biochemical, chemical, and genetic experiments revealed that on-target blockade of the HDAC1/2 catalytic domain mediated the differentiated phenotype.
View Article and Find Full Text PDFPleura Peritoneum
December 2024
Faculty of Health, Aarhus University, Aarhus, Denmark.
Objectives: Cancer cells can activate coagulation and inhibit fibrinolysis. The aim was to investigate the association between the burden of peritoneal metastases from colorectal cancer (PM-CRC) and biomarkers reflecting thrombin generation and fibrinolysis.
Methods: A cohort of 55 patients with PM-CRC scheduled for cytoreductive surgery.
Int J Gen Med
December 2024
Department of Gastroenterology, Meizhou People's Hospital, Meizhou, People's Republic of China.
Background: Susceptibility to some cancers is linked to methylenetetrahydrofolate reductase () polymorphisms and the Controlling Nutritional Status (CONUT) score in some populations. However, their relationship with susceptibility to colorectal cancer (CRC) susceptibility in the Hakka Chinese population remains unclear.
Methods: In total, 620 CRC patients and 734 controls were enrolled.
Front Immunol
December 2024
Department of Gastrointestinal Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Background: Hypoxia in the tumor microenvironment (TME) plays a pivotal role in the progression and prognosis of colorectal cancer (CRC). However, effective methods for assessing TME hypoxia remain lacking. This study aims to develop a novel hypoxia-related prognostic score (HPS) based on hypoxia-associated genes to improve CRC prognostication and inform treatment strategies.
View Article and Find Full Text PDFFront Oncol
December 2024
Department of Integrative Translational Sciences, City of Hope, Beckman Research Institute, Duarte, CA, United States.
Over the past century, colorectal cancer (CRC) has become one of the most devastating cancers impacting the human population. To gain a deeper understanding of the molecular mechanisms driving this solid tumor, researchers have increasingly turned their attention to the tumor microenvironment (TME). Spatial transcriptomics and proteomics have emerged as a particularly powerful technology for deciphering the complexity of CRC tumors, given that the TME and its spatial organization are critical determinants of disease progression and treatment response.
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