Category Ranking

98%

Total Visits

921

Avg Visit Duration

2 minutes

Citations

20

Article Abstract

RNA interactomes and their diversified functionalities have recently benefited from critical methodological advances leading to a paradigm shift from a conventional conception on the regulatory roles of RNA in pathogenesis. However, the dynamic RNA interactomes in adenoma-carcinoma sequence of human CRC remain unexplored. The coexistence of adenoma, cancer, and normal tissues in colorectal cancer (CRC) patients provides an appropriate model to address this issue. Here, we adopted an RNA in situ conformation sequencing technology for mapping RNA-RNA interactions in CRC patients. We observed large-scale paired RNA counts and identified some unique RNA complexes including multiple partners RNAs, single partner RNAs, non-overlapping single partner RNAs. We focused on the antisense RNA OIP5-AS1 and found that OIP5-AS1 could sponge different miRNA to regulate the production of metabolites including pyruvate, alanine and lactic acid. Our findings provide novel perspectives in CRC pathogenesis and suggest metabolic reprogramming of pyruvate for the early diagnosis and treatment of CRC.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11106987PMC
http://dx.doi.org/10.1186/s12885-024-12367-7DOI Listing

Publication Analysis

Top Keywords

metabolic reprogramming
8
reprogramming pyruvate
8
colorectal cancer
8
rna interactomes
8
crc patients
8
single partner
8
partner rnas
8
rna
7
crc
5
selective sponging
4

Similar Publications

Cadmium (Cd) is a heavy metal that exhibits strong carcinogenic properties and promotes breast cancer (BC) progression. Autophagic flux dysfunction is involved in Cd-induced BC progression, but the underlying molecular mechanisms remain unclear. Here, it is observed that impaired autophagic flux and metabolic reprogramming are notable features related to Cd-induced proliferation, migration, and invasion in BC cell lines, including T-47D and MCF-7 cells.

View Article and Find Full Text PDF

Background: The clinical differentiation between obstetric antiphospholipid syndrome (OAPS) and undifferentiated connective tissue disease (UCTD) presents significant diagnostic challenges. This study employs metabolomics to investigate metabolic reprogramming patterns in OAPS and UCTD, aiming to identify potential biomarkers for early diagnosis.

Methods: Using LC-MS-based metabolomics, we analyzed serum profiles from 40 OAPS patients (B1), 30 OAPS + UCTD patients (B2), 27 UCTD patients (B3), and 30 healthy controls (A1).

View Article and Find Full Text PDF

Organelle stresses and energetic metabolisms promote endothelial-to-mesenchymal transition and fibrosis via upregulating FOSB and MEOX1 in Alzheimer's disease.

Front Mol Neurosci

August 2025

Department of Cardiovascular Sciences, Lewis Katz School of Medicine, Lemole Center for Integrated Lymphatics and Vascular Research, Temple University, Philadelphia, PA, United States.

Introduction: Endothelial-to-mesenchymal transition (EndoMT), cell death, and fibrosis are increasingly recognized as contributing factors to Alzheimer's disease (AD) pathology, but the underlying transcriptomic mechanisms remain poorly defined. This study aims to elucidate transcriptomic changes associated with EndoMT, diverse cell death pathways, and fibrosis in AD using the 3xTg-AD mouse model.

Methods: Using RNA-seq data and knowledge-based transcriptomic analysis on brain tissues from the 3xTg-AD mouse model of AD.

View Article and Find Full Text PDF

Background: Feline panleukopenia, caused by the highly lethal feline parvovirus (FPV), lacks effective prevention and treatment strategies. This study aimed to elucidate the key metabolic regulatory mechanisms during FPV infection.

Methods: CRFK cells were infected with the FPV013 strain.

View Article and Find Full Text PDF

Ferroptosis, an iron-dependent cell death pathway driven by lipid peroxidation, has emerged as a critical pathophysiological mechanism linking cancer and inflammatory diseases. The seemingly distinct pathologies exhibit shared microenvironmental hallmarks-oxidative stress, immune dysregulation, and metabolic reprogramming-that converge on ferroptosis regulation. This review synthesizes how ferroptosis operates at the intersection of these diseases, acting as both a tumor-suppressive mechanism and a driver of inflammatory tissue damage.

View Article and Find Full Text PDF