NAT10 Phase Separation Regulates YTHDF1 Splicing to Promote Gastric Cancer Progression.

Gastric cancer is an aggressive malignancy with poor patient outcomes. N-Acetyltransferase 10 (NAT10) is an acetyltransferase that has been reported to contribute to gastric cancer progression. In-depth investigation into the underlying molecular mechanisms driven by NAT10 could help identify therapeutic targets to improve gastric cancer treatment.

Modulation of YBX1-mediated PANoptosis inhibition by PPM1B and USP10 confers chemoresistance to oxaliplatin in gastric cancer.

Gastric cancer (GC) is a common malignant tumor of the digestive tract, and chemoresistance significantly impacts GC patients' prognosis. PANoptosis has been associated with oxaliplatin-induced cell death. However, the direct regulatory role of YBX1 in cellular chemoresistance through PANoptosis remains unclear.

SLC26A3/NHERF2-IκB/NFκB/p65 feedback loop suppresses tumorigenesis and metastasis in colorectal cancer.

Colorectal cancer (CRC) is a formidable disease due to the intricate mechanisms that drive its proliferation and metastasis. Despite significant progress in cancer research, the integration of these mechanisms that influence cancer cell behavior remains elusive. Therefore, it is imperative to comprehensively elucidate the underlying mechanisms driving CRC proliferation and metastasis.

Screening of hub inflammatory bowel disease biomarkers and identification of immune-related functions based on basement membrane genes.

Background: Inflammatory bowel disease (IBD), including Crohn's disease (CD) and ulcerative colitis (UC), is a chronic, inflammatory, and autoimmune disease, but its specific etiology and pathogenesis are still unclear. This study aimed to better discover the causative basement membrane (BM) genes of their subtypes and their associations.

Methods: The differential expression of BM genes between CD and UC was analyzed and validated by downloading relevant datasets from the GEO database.

Bioinformatics Analysis of Immune Infiltration In Endometrial Carcinoma Tumors and its Relationship With Prognosis.

Background/aim: Endometrial carcinoma (EC) is the most common gynecological cancer, but lacks specific targetable markers. In order to explore the immune-related molecules that affect the progression and prognosis of EC, we analyzed the differential expression of genes in different histological grades of the disease.

Materials And Methods: EC-related gene-expression data of different histological grades were downloaded from TCGA and GEO databases.

Analysis of the characteristics of immune infiltration in endometrial carcinoma and its relationship with prognosis based on bioinformatics.

To explore immune-related molecules that affect the prognosis of endometrial carcinoma (EC) using bioinformatic data mining. The expression data related to EC were downloaded from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus databases. After differential expression analysis, the intersection with immune related genes in the ImmPort database was used to obtain immune related differentially expressed genes (IRDEGs).

TRAF6 regulates the abundance of RIPK1 and inhibits the RIPK1/RIPK3/MLKL necroptosis signaling pathway and affects the progression of colorectal cancer.

Colorectal cancer cannot be completely cured at present, and it is still an important clinical medical problem. TRAF6 is highly expressed in many malignant tumors. However, the role of TRAF6 in colorectal cancer is still controversial, mainly because the specific regulatory mechanism of colorectal cancer is still unclear, and the death mode of colorectal cancer cells has not been elucidated.

KLRF1, a novel marker of CD56 NK cells, predicts improved survival for patients with locally advanced bladder cancer.

Background: Bladder tumor-infiltrating CD56 NK cells are more tumor cytotoxic than their CD56 counterparts. Identification of NK cell subsets is labor-intensive and has limited utility in the clinical setting. Here, we sought to identify a surrogate marker of bladder CD56 NK cells and to test its prognostic significance.

TRAF6 regulates the signaling pathway influencing colorectal cancer function through ubiquitination mechanisms.

Tumor necrosis factor receptor-associated factor-6 (TRAF6) is a ubiquitin E3 ligase. TRAF6 plays an important role in tumor invasion and metastasis. However, the specific mechanism by which TRAF6 promotes colorectal cancer (CRC) metastasis is incompletely understood.

2-Hydroxyglutarate destabilizes chromatin regulatory landscape and lineage fidelity to promote cellular heterogeneity.

The epigenome delineates lineage-specific transcriptional programs and restricts cell plasticity to prevent non-physiological cell fate transitions. Although cell diversification fosters tumor evolution and therapy resistance, upstream mechanisms that regulate the stability and plasticity of the cancer epigenome remain elusive. Here we show that 2-hydroxyglutarate (2HG) not only suppresses DNA repair but also mediates the high-plasticity chromatin landscape.

Bladder tumor ILC1s undergo Th17-like differentiation in human bladder cancer.

Purpose: Human innate lymphoid cells (hILCs) are lineage-negative immune cells that do not express rearranged adaptive antigen receptors. Natural killer (NK) cells are hILCs that contribute to cancer defense. The role of non-NK hILCs in cancer is unclear.

Contacts with Macrophages Promote an Aggressive Nanomechanical Phenotype of Circulating Tumor Cells in Prostate Cancer.

Aggressive tumors of epithelial origin shed cells that intravasate and become circulating tumor cells (CTC). The CTCs that are able to survive the stresses encountered in the bloodstream can then seed metastases. We demonstrated previously that CTCs isolated from the blood of prostate cancer patients display specific nanomechanical phenotypes characteristic of cell endurance and invasiveness and patient sensitivity to androgen deprivation therapy.

Vimentin affects colorectal cancer proliferation, invasion, and migration via regulated by activator protein 1.

Uncontrolled recurrence and metastasis are important reasons for the high mortality rate of malignant tumors. Vimentin is positively correlated with the degree of malignancy of cancer cells. Vimentin is also highly expressed in colorectal cancer (CRC) cells and plays a critical role in the metastasis and prognosis of CRC.

The Effects of on Growth and Progression in Colorectal Cancer are Regulated by .

Background And Aim: Some studies have confirmed that exhibits a suppressive role in gastric cancer, Wilms' tumor. However, the function of in colorectal cancer has not been completely elucidated. The present study aims to verify as the targeted gene by which was investigated in colorectal cancer tissues and cells, and its effects on the biological characteristics of colorectal cancer cells were determined, in order to provide an experimental and theoretical basis for the application of in the treatment of colorectal cancer.

PAI-1-Dependent Inactivation of SMAD4-Modulated Junction and Adhesion Complex in Obese Endometrial Cancer.

While plasminogen activator inhibitor-1 (PAI-1) is known to potentiate cellular migration via proteolytic regulation, this adipokine is implicated as an oncogenic ligand in the tumor microenvironment. To understand the underlying paracrine mechanism, here, we conduct transcriptomic analysis of 1,898 endometrial epithelial cells (EECs) exposed and unexposed to PAI-1-secreting adipose stromal cells. The PAI-1-dependent action deregulates crosstalk among tumor-promoting and tumor-repressing pathways, including transforming growth factor β (TGF-β).

Novel visualized quantitative epigenetic imprinted gene biomarkers diagnose the malignancy of ten cancer types.

Background: Epigenetic alterations are involved in most cancers, but its application in cancer diagnosis is still limited. More practical and intuitive methods to detect the aberrant expressions from clinical samples using highly sensitive biomarkers are needed. In this study, we developed a novel approach in identifying, visualizing, and quantifying the biallelic and multiallelic expressions of an imprinted gene panel associated with cancer status.

ERα-related chromothripsis enhances concordant gene transcription on chromosome 17q11.1-q24.1 in luminal breast cancer.

Background: Chromothripsis is an event of genomic instability leading to complex chromosomal alterations in cancer. Frequent long-range chromatin interactions between transcription factors (TFs) and targets may promote extensive translocations and copy-number alterations in proximal contact regions through inappropriate DNA stitching. Although studies have proposed models to explain the initiation of chromothripsis, few discussed how TFs influence this process for tumor progression.

m A RNA methylation regulators contribute to malignant progression in rectal cancer.

N6,2'-O-dimethyladenosine (m A) RNA methylation, which is correlated with cancer initiation and progression, is dynamically regulated by m A RNA methylation regulators, including writers, erasers, and readers. Two subgroups of rectal cancer, including cluster1 and cluster2, were identified based on consensus clustering to m A RNA methylation regulators. A protein-protein interaction network was constructed and hub genes were identified.

Operable gastric adenocarcinoma with different histological subtypes: Cancer-specific survival in the United States.

Background/aims: Gastric signet ring cell carcinoma (GSRC), a subtype of adenocarcinoma, has been considered a histological type with poor survival. We aimed to compare the survival outcomes between patients with GSRC and patients with gastric non-signet ring cell adenocarcinoma (NGSRC) and constructed a nomogram to predict gastric adenocarcinoma-specific survival (GCSS).

Patients And Methods: We identified 10,031 patients with gastric adenocarcinoma (GA) from the surveillance, epidemiology, and end results (SEER) database and stratified them into two histological type groups: GSRC and NGSRC.

Single-Cell Proteomic Profiling Identifies Combined AXL and JAK1 Inhibition as a Novel Therapeutic Strategy for Lung Cancer.

Cytometry by time-of-flight (CyTOF) simultaneously measures multiple cellular proteins at the single-cell level and is used to assess intertumor and intratumor heterogeneity. This approach may be used to investigate the variability of individual tumor responses to treatments. Herein, we stratified lung tumor subpopulations based on AXL signaling as a potential targeting strategy.

TRAF6-Mediated Inflammatory Cytokines Secretion in LPS-induced Colorectal Cancer Cells Is Regulated by miR-140.

Background/aim: Colorectal cancer (CRC) cells secrete inflammatory cytokines that affect CRC progression. The aim of the present study was to determine if micro-RNA-140(miR-140) regulates inflammatory cytokine secretion induced by lipopolysaccharide (LPS) in colorectal cancer cells by targeting tumor necrosis factor receptor (TNFR)-associated factor 6 (TRAF6).

Materials And Methods: Fifty fresh colon-cancer specimens and normal colorectal tissues were collected from patients with CRC and tested for the expression miR-140.

Spatial EGFR Dynamics and Metastatic Phenotypes Modulated by Upregulated EphB2 and Src Pathways in Advanced Prostate Cancer.

Advanced prostate cancer is a very heterogeneous disease reflecting in diverse regulations of oncogenic signaling pathways. Aberrant spatial dynamics of epidermal growth factor receptor (EGFR) promote their dimerization and clustering, leading to constitutive activation in oncogenesis. The EphB2 and Src signaling pathways are associated with the reorganization of the cytoskeleton leading to malignancy, but their roles in regulating EGFR dynamics and activation are scarcely reported.

MyD88 mediates colorectal cancer cell proliferation, migration and invasion via NF‑κB/AP‑1 signaling pathway.

The role of myeloid differentiation factor 88 (MyD88) in malignant tumors is largely unknown. Therefore, in this study, we aimed to examine the function and underlying mechanism of MyD88 in colorectal carcinoma in vitro using SW480 and HCT116 cell lines and in vivo using a nude mouse model. SW480 and HCT116 cells were infected with a lentiviral‑based effective MyD88 siRNA virus.