Cellular senescence gene TACC3 associated with colorectal cancer risk via genetic and DNA methylated alteration.

Cell senescence genes play a vital role in the pathogenesis of colorectal cancer, a process that may involve the triggering of genetic variations and reversible phenotypes caused by epigenetic modifications. However, the specific regulatory mechanisms remain unclear. Using CellAge and The Cancer Genome Atlas databases and in-house RNA-seq data, DNA methylation-modified cellular senescence genes (DMCSGs) were validated by Support Vector Machine and correlation analyses.

Unveiling immunogenic cell death-related genes in colorectal cancer: an integrated study incorporating transcriptome and Mendelian randomization analyses.

Immunogenic cell death (ICD), a type of cell death that activates the tumor-specific immune response and thus exerts anti-tumor effects, is an emerging target in tumor therapy, but research on ICD-related genes (ICDGs) in colorectal cancer (CRC) remains limited. This study aimed to identify the CRC-specific ICDGs and explore their potential roles. Through RNA sequencing for tissue samples from CRC patients and integration with The Cancer Genome Atlas (TCGA) data, we identified 33 differentially expressed ICDGs in CRC.

Machine learning-based glycolysis-associated molecular classification reveals differences in prognosis, TME, and immunotherapy for colorectal cancer patients.

Background: Aerobic glycolysis is a process that metabolizes glucose under aerobic conditions, finally producing pyruvate, lactic acid, and ATP for tumor cells. Nevertheless, the overall significance of glycolysis-related genes in colorectal cancer and how they affect the immune microenvironment have not been investigated.

Methods: By combining the transcriptome and single-cell analysis, we summarize the various expression patterns of glycolysis-related genes in colorectal cancer.

Promotes Proliferation and Metastasis by Targeting Hippo/YAP Signalling in Colorectal Cancer.

The complex in which scribble planar cell polarity protein () is located is one of the three main polar protein complexes that play an important role in maintaining epithelial polarity and affecting tumour growth. However, the role of in colorectal cancer (CRC) remains largely unknown. This study used date from The Cancer Genome Atlas (TCGA) and clinical samples to determine the expression of in CRC and explored its mechanism through bioinformatics analysis and and experiments.

Hypoxic colorectal cancer-derived extracellular vesicles deliver microRNA-361-3p to facilitate cell proliferation by targeting TRAF3 via the noncanonical NF-κB pathways.

Background: Hypoxic tumour microenvironment (TME) is a key regulator in cancer progression. However, the communications between hypoxic cells and other components in TME during colorectal cancer (CRC) progression via extracellular vesicles (EVs) remain unclear.

Methods: High-throughput sequencing was employed to detect aberrantly expressed microRNAs (miRNAs) in hypoxic EVs.

Genetic variants in Hippo signalling pathway-related genes affect the risk of colorectal cancer.

The Hippo signalling pathway plays a crucial role in carcinogenesis. Therefore, we hypothesized that genetic variants in genes related to this pathway are associated with the colorectal cancer risk. A case-control study including 1150 patients and 1342 controls was performed to assess the association of genetic variants of genes involved in the Hippo signalling pathway with the risk of colorectal cancer.

RFC2, a direct target of miR-744, modulates the cell cycle and promotes the proliferation of CRC cells.

Colorectal cancer (CRC) is a common digestive tract malignancy, which is characterized by high mortality, morbidity, and poor prognosis. Replication factor C subunit 2 (RFC2), one RFC family member, was reported to be related to various malignancies and plays an important role in proliferation, invasion, and metastasis. Nonetheless, the RFC2 biological role within CRC is still unknown.