Transcription factor ZEB1 coordinating with NuRD complex to promote oncogenesis through glycolysis in colorectal cancer.

Background: Colorectal cancer (CRC) is an aggressive primary intestinal malignancy with the third-highest incidence and second-highest mortality among all cancer types worldwide. Transcription factors (TFs) regulate cell development and differentiation owing to their ability to recognize specific DNA sequences upstream of genes. Numerous studies have demonstrated a strong correlation between TFs, the etiology of tumors, and therapeutic approaches.

Prognostic analysis of patients with gastric cancer based on N-methyladenosine modification patterns and tumor microenvironment characterization.

Background: Cancers arise from genetic and epigenetic abnormalities that affect oncogenes and tumor suppressor genes, compounded by gene mutations. The N6-methyladenosine (mA) RNA modification, regulated by methylation regulators, has been implicated in tumor proliferation, differentiation, tumorigenesis, invasion, and metastasis. However, the role of mA modification patterns in the tumor microenvironment of gastric cancer (GC) remains poorly understood.

The feedback loop between MTA1 and MTA3/TRIM21 modulates stemness of breast cancer in response to estrogen.

The metastasis-associated protein (MTA) family plays a crucial role in the development of breast cancer, a common malignancy with a high incidence rate among women. However, the mechanism by which each member of the MTA family contributes to breast cancer progression is poorly understood. In this study, we aimed to investigate the roles of MTA1, MTA3, and tripartite motif-containing 21 (TRIM21) in the proliferation, invasion, epithelial-mesenchymal transition (EMT), and stem cell-like properties of breast cancer cells in vivo and in vitro.

The E3 ligase TRIM22 functions as a tumor suppressor in breast cancer by targeting CCS for proteasomal degradation to inhibit STAT3 signaling.

Deregulation of E3 ubiquitin ligases drives the proliferation and metastasis of various cancers; however, the underlying mechanisms remain unknown. This study aimed to investigate the role of tripartite motif-containing 22 (TRIM22), a poorly investigated E3 ubiquitin ligase in the TRIM family, as a tumor suppressor in breast cancer. High expression of TRIM22 in breast cancer correlated with better prognosis.

CARM1 drives triple-negative breast cancer progression by coordinating with HIF1A.

Coactivator-associated arginine methyltransferase 1 (CARM1) promotes the development and metastasis of estrogen receptor alpha (ERα)-positive breast cancer. The function of CARM1 in triple-negative breast cancer (TNBC) is still unclear and requires further exploration. Here, we report that CARM1 promotes proliferation, epithelial-mesenchymal transition, and stemness in TNBC.

JARID2 coordinates with the NuRD complex to facilitate breast tumorigenesis through response to adipocyte-derived leptin.

Background: Proteins containing the Jumonji C (JmjC) domain participated in tumorigenesis and cancer progression. However, the mechanisms underlying this effect are still poorly understood. Our objective was to investigate the role of Jumonji and the AT-rich interaction domain-containing 2 (JARID2) - a JmjC family protein - in breast cancer, as well as its latent association with obesity.

Prognostic analysis of patients with breast cancer based on tumor mutational burden and DNA damage repair genes.

Background: Breast cancer has a high tumor-specific death rate and poor prognosis. In this study, we aimed to provide a basis for the prognostic risk in patients with breast cancer using significant gene sets selected by analyzing tumor mutational burden (TMB) and DNA damage repair (DDR).

Methods: Breast cancer genomic and transcriptomic data were obtained from The Cancer Genome Atlas (TCGA).

Identifying key transcription factors and immune infiltration in non-small-cell lung cancer using weighted correlation network and Cox regression analyses.

Introduction: Lung cancer is one of the most common cancers and a significant cause of cancer-related deaths. Non-small cell lung cancer (NSCLC) accounts for about 85% of all lung cancer cases. Therefore, it is crucial to identify effective diagnostic and therapeutic methods.

The PRMT6/PARP1/CRL4B Complex Regulates the Circadian Clock and Promotes Breast Tumorigenesis.

Circadian rhythms, as physiological systems with self-regulatory functions in living organisms, are controlled by core clock genes and are involved in tumor development. The protein arginine methyltransferase 6 (PRMT6) serves as an oncogene in a myriad of solid tumors, including breast cancer. Hence, the primary aim of the current study is to investigate the molecular mechanisms by which the PRMT6 complex promotes breast cancer progression.

mA regulators featured by tumor immune microenvironment landscapes and correlated with immunotherapy in non-small cell lung cancer (NSCLC).

Introduction: Recent research has confirmed the critical role that epigenetic factors play in regulating the immune response. Nonetheless, what role mA methylation modification might play in the immune response of non-small cell lung cancer (NSCLC) remains vague.

Methods: Herein, the gene expression, copy number variations (CNVs), and somatic mutations of 31 mA regulators in NSCLC and adjacent control samples from the GEO and TCGA databases were comprehensively explored.

RUNX2 recruits the NuRD(MTA1)/CRL4B complex to promote breast cancer progression and bone metastasis.

Runt-related transcription factor 2 (RUNX2) is an osteogenesis-related transcription factor that has emerged as a prominent transcription repressing factor in carcinogenesis. However, the role of RUNX2 in breast cancer metastasis remains poorly understood. Here, we show that RUNX2 recruits the metastasis-associated 1 (MTA1)/NuRD and the Cullin 4B (CUL4B)-Ring E3 ligase (CRL4B) complex to form a transcriptional-repressive complex, which catalyzes the histone deacetylation and ubiquitylation.

The hub ten gene-based risk score system using RNA mA methylation regulator features and tumor immune microenvironment in breast cancer.

Background: RNA N-methyladenosine (mA) modification is primarily regulated by mA regulators, which play significant epigenetic regulatory roles in tumorigenesis, tumor development, and tumor immune microenvironment. However, the correlation between mA regulators and immune cell infiltration in breast cancer remains unclear.

Methods: In this study, mA modification patterns were evaluated based on 31 mA modification regulators.

Identification of Key Transcription Factors and Immune Infiltration Patterns Associated With Breast Cancer Prognosis Using WGCNA and Cox Regression Analysis.

Breast cancer is the most frequently diagnosed cancer and the second leading cause of cancer death among women worldwide. Therefore, the need for effective breast cancer treatment is urgent. Transcription factors (TFs) directly participate in gene transcription, and their dysregulation plays a key role in breast cancer.

BCAS3 exhibits oncogenic properties by promoting CRL4A-mediated ubiquitination of p53 in breast cancer.

Objectives: Breast cancer-amplified sequence 3 (BCAS3) was initially found to be amplified in human breast cancer (BRCA); however, there has been little consensus on the functions of BCAS3 in breast tumours.

Materials And Methods: We analysed BCAS3 expression in BRCA using bio-information tools. Affinity purification and mass spectrometry were employed to identify BCAS3-associated proteins.

Snail/PRMT5/NuRD complex contributes to DNA hypermethylation in cervical cancer by TET1 inhibition.

The biological function of PRMT5 remains poorly understood in cervical cancer metastasis. Here, we report that PRMT5 physically associates with the transcription factor Snail and the NuRD(MTA1) complex to form a transcriptional-repressive complex that catalyzes the symmetrical histone dimethylation and deacetylation. This study shows that the Snail/PRMT5/NuRD(MTA1) complex targets genes, such as TET1 and E-cadherin, which are critical for epithelial-mesenchymal transition (EMT).

A Ten-N-Methyladenosine (mA)-Modified Gene Signature Based on a Risk Score System Predicts Patient Prognosis in Rectum Adenocarcinoma.

Objectives: The study aims to analyze the expression of N-methyladenosine (mA)-modified genes in rectum adenocarcinoma (READ) and identify reliable prognostic biomarkers to predict the prognosis of READ.

Materials And Methods: RNA sequence data of READ and corresponding clinical survival data were obtained from The Cancer Genome Atlas (TCGA) database. N-methyladenosine (mA)-modified genes in READ were downloaded from the "m6Avar" database.

The histone deacetylase inhibitor PCI-24781 impairs calcium influx and inhibits proliferation and metastasis in breast cancer.

Histone deacetylases (HDACs) are involved in key cellular processes and have been implicated in cancer. As such, compounds that target HDACs or drugs that target epigenetic markers may be potential candidates for cancer therapy. This study was therefore aimed to identify a potential epidrug with low toxicity and high efficiency as anti-tumor agents.

Identification of key modules and genes associated with breast cancer prognosis using WGCNA and ceRNA network analysis.

Breast cancer is one of the leading causes of cancer-associated mortality in women worldwide and has become a major public health problem. Although the definitive cause of breast cancer is not known, many genes sensitive to breast cancer have been detected using advanced technologies. Our study identified 3301 differentially expressed lncRNAs and mRNAs between tumor and normal samples from The Cancer Genome Atlas database.

Exploring TCGA database for identification of potential prognostic genes in stomach adenocarcinoma.

Background: Stomach adenocarcinoma (STAD) is the fifth most prevalent cancer in the world and ranks third among cancer-related deaths worldwide. The tumour microenvironment (TME) plays an important role in tumorigenesis, development, and metastasis. Hence, we calculated the immune and stromal scores to find the potential prognosis-related genes in STAD using bioinformatics analysis.

PHF20L1 as a H3K27me2 reader coordinates with transcriptional repressors to promote breast tumorigenesis.

TUDOR domain-containing proteins (TDRDs) are chiefly responsible for recognizing methyl-lysine/arginine residue. However, how TDRD dysregulation contributes to breast tumorigenesis is poorly understood. Here, we report that TUDOR domain-containing PHF20L1 as a H3K27me2 reader exerts transcriptional repression by recruiting polycomb repressive complex 2 (PRC2) and Mi-2/nucleosome remodeling and deacetylase (NuRD) complex, linking PRC2-mediated methylation and NuRD-mediated deacetylation of H3K27.

GATA3 recruits UTX for gene transcriptional activation to suppress metastasis of breast cancer.

GATA3 has emerged as a prominent transcription factor required for maintaining mammary-gland homeostasis. GATA3 loss is associated with aggressive breast cancer development, but the mechanism by which breast cancer is affected by the loss of GATA3 function remains unclear. Here, we report that GATA3 expression is positively correlated with the expression of UTX, a histone H3K27 demethylase contained in the MLL4 methyltransferase complex, and that GATA3 recruits the chromatin-remodeling MLL4 complex and interacts directly with UTX, ASH2L, and RBBP5.

MicroRNA-455-3p mediates GATA3 tumor suppression in mammary epithelial cells by inhibiting TGF-β signaling.

GATA3 is a basic and essential transcription factor that regulates many pathophysiological processes and is required for the development of mammary luminal epithelial cells. Loss-of-function GATA3 alterations in breast cancer are associated with poor prognosis. Here, we sought to understand the tumor-suppressive functions GATA3 normally performs.

Differential expression and functions of Ehm2 transcript variants in lung adenocarcinoma.

Ehm2 [also known as erythrocyte membrane protein band 4.1‑like protein 4B (EPB41L4B)] is a member of the NF2/ERM/4.1 superfamily.

Cystatin C Expression is Promoted by VEGFA Blocking, With Inhibitory Effects on Endothelial Cell Angiogenic Functions Including Proliferation, Migration, and Chorioallantoic Membrane Angiogenesis.

Background Vascular development, including vasculogenesis and angiogenesis, is involved in many diseases. Cystatin C ( CST 3) is a commonly used marker of renal dysfunction, and we have previously reported that its expression level is associated with variations in the gerbil circle of Willis. Thus, we hypothesized that CST 3 may affect endothelial function and angiogenic capacity.