BACH1 controls hepatic insulin signaling and glucose homeostasis in mice.

Hepatic insulin resistance is central to the metabolic syndrome. Here we investigate the role of BTB and CNC homology 1 (BACH1) in hepatic insulin signaling. BACH1 is elevated in the hepatocytes of individuals with obesity and patients with non-alcoholic fatty liver disease (NAFLD).

BACH1 regulates the differentiation of vascular smooth muscle cells from human embryonic stem cells via CARM1-mediated methylation of H3R17.

The role of BACH1 in the process of vascular smooth muscle cell (VSMC) differentiation from human embryonic stem cells (hESCs) remains unknown. Here, we find that the loss of BACH1 in hESCs attenuates the expression of VSMC marker genes, whereas overexpression of BACH1 after mesoderm induction increases the expression of VSMC markers during in vitro hESC-VSMC differentiation. Mechanistically, BACH1 binds directly to coactivator-associated arginine methyltransferase 1 (CARM1) during in vitro hESC-VSMC differentiation, and this interaction is mediated by the BACH1 bZIP domain.

Cardiac-specific BACH1 ablation attenuates pathological cardiac hypertrophy by inhibiting the Ang II type 1 receptor expression and the Ca2+/CaMKII pathway.

Aims: BACH1 is up-regulated in hypertrophic hearts, but its function in cardiac hypertrophy remains largely unknown. This research investigates the function and mechanisms of BACH1 in the regulation of cardiac hypertrophy.

Methods And Results: Male cardiac-specific BACH1 knockout mice or cardiac-specific BACH1 transgenic (BACH1-Tg) mice and their respective wild-type littermates developed cardiac hypertrophy induced by angiotensin II (Ang II) or transverse aortic constriction (TAC).

Head-to-Head Comparison of the Expression Differences of NECTIN-4, TROP-2, and HER2 in Urothelial Carcinoma and Its Histologic Variants.

Background: Antibody-drug conjugates (ADC), such as enfortumab vedotin (EV), sacituzumab govitecan (SG), and RC-48, have shown outstanding response rates to local advanced or metastatic urothelial carcinoma (UC). However, their corresponding target expression characteristics in UC and its histologic variants were unknown.

Methods: We detected the expression of NECTIN-4, TROP-2, and HER2, which are the corresponding targets of ADCs EV, SG, and RC-48 in muscle-invasive UC through immunohistochemistry.

Deletion of BACH1 Attenuates Atherosclerosis by Reducing Endothelial Inflammation.

Background: The transcription factor BACH1 (BTB and CNC homology 1) suppressed endothelial cells (ECs) proliferation and migration and impaired angiogenesis in the ischemic hindlimbs of adult mice. However, the role and underlying mechanisms of BACH1 in atherosclerosis remain unclear.

Methods: Mouse models of atherosclerosis in endothelial cell (EC)-specific-Bach1 knockout mice were used to study the role of BACH1 in the regulation of atherogenesis and the underlying mechanisms.

mA-mRNA Methylation Regulates Gene Expression and Programmable mA Modification of Cellular RNAs With CRISPR-Cas13b in Renal Cell Carcinoma.

N-methyladenosine (mA) is the most extensive messenger RNA modification. Despite recent advances in the biological roles of mA, its role in the development and progression of renal cell carcinoma (RCC) remains unclear. In this study, we gained the transcriptome-wide mA profile and gene expression pattern in RCC and paired adjacent peritumoral tissues by meRIP-seq and RNA-seq.

Identifying a hypoxia related score to predict the prognosis of bladder cancer: a study with The Cancer Genome Atlas (TCGA) database.

Background: Recurrence is common in bladder cancer, with a hypoxic tumor microenvironment (TME) playing a role in genetic instability and prognosis of bladder cancer. However, we still lack practical hypoxia related model for predicting the prognosis of bladder cancer. In this study, we identified new prognosis-related hypoxia genes and established a new hypoxia score related signature.

Carbonic anhydrase 10 functions as a tumor suppressor in renal cell carcinoma and its methylation is a risk factor for survival outcome.

Carbonic anhydrase 10 (CA10), one of the carbonic anhydrase isozymes, is explored to be downregulated in several tumor types, which indicates its critical role in tumorigenesis. However, its biologic and pathological function remains elusive in the pathogenesis of renal cell carcinoma (RCC). We examined expressions and functions of CA10 in RCC primary tumors and cell lines, assessed its tumor suppressive functions and further explored its impact on survival outcome of RCC patients.

Identifying Hypoxia Characteristics to Stratify Prognosis and Assess the Tumor Immune Microenvironment in Renal Cell Carcinoma.

Renal cell carcinoma (RCC) is a common malignant tumor worldwide, and immune checkpoint inhibitors are a new therapeutic option for metastatic RCC. Infiltrating immune cells in the tumor microenvironment (TME) play a critical part in RCC biology, which is important for tumor therapy and prediction. Hypoxia is a common condition that occurs in the TME and may lead to RCC immunosuppression and immune escape.

Renal Ewing's sarcoma/primitive neuroectodermal tumor (PNET): a case series of 7 patients and literature review.

Background: Primitive neuroectodermal tumor (PNET) is a rare kind of sarcoma that is primarily found in the kidney and has a very poor prognosis. Here, we review and summarize the clinical data of patients with renal PNET in our center and follow up the patients for survival status. Although the current literature suggests that chemotherapy may benefit the survival of these patients, the information from our center suggests that this may not be the case.

Epigenetic Alterations in Renal Cell Cancer With TKIs Resistance: From Mechanisms to Clinical Applications.

The appearance of tyrosine kinase inhibitors (TKIs) has been a major breakthrough in renal cell carcinoma (RCC) therapy. Unfortunately, a portion of patients with TKIs resistance experience disease progression after TKIs therapy. Epigenetic alterations play an important role in the development of TKIs resistance.

Single-cell RNA analysis on ACE2 expression provides insights into SARS-CoV-2 potential entry into the bloodstream and heart injury.

Coronavirus disease-2019 (COVID-19) is a global pandemic with high infectivity and pathogenicity, accounting for tens of thousands of deaths worldwide. Recent studies have found that the pathogen of COVID-19, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), shares the same cell receptor angiotensin converting enzyme II (ACE2) as SARS-CoV. The pathological investigation of COVID-19 deaths showed that the lungs had characteristics of pulmonary fibrosis.

Bach1-induced suppression of angiogenesis is dependent on the BTB domain.

The transcription factor Bach1 impairs angiogenesis after ischemic injury by suppressing Wnt/β-catenin signaling; however, the specific domains responsible for the anti-angiogenic effects of Bach1 remain unclear. This study determined the role of the BTB domain of Bach1 in ischemic angiogenesis. Bach1 is highly expressed in circulating endothelial cells from acute myocardial infarction patients and is the early induction gene after ischemia.

Bach1 regulates self-renewal and impedes mesendodermal differentiation of human embryonic stem cells.

The transcription factor BTB and CNC homology 1 (Bach1) is expressed in the embryos of mice, but whether Bach1 regulates the self-renewal and early differentiation of human embryonic stem cells (hESCs) is unknown. We report that the deubiquitinase ubiquitin-specific processing protease 7 (Usp7) is a direct target of Bach1, that Bach1 interacts with Nanog, Sox2, and Oct4, and that Bach1 facilitates their deubiquitination and stabilization via the recruitment of Usp7, thereby maintaining stem cell identity and self-renewal. Bach1 also interacts with polycomb repressive complex 2 (PRC2) and represses mesendodermal gene expression by recruiting PRC2 to the genes' promoters.

Bach1: Function, Regulation, and Involvement in Disease.

The transcription factor BTB and CNC homology 1 (Bach1) is widely expressed in most mammalian tissues and functions primarily as a transcriptional suppressor by heterodimerizing with small Maf proteins and binding to Maf recognition elements in the promoters of targeted genes. It has a key regulatory role in the production of reactive oxygen species, cell cycle, heme homeostasis, hematopoiesis, and immunity and has been shown to suppress ischemic angiogenesis and promote breast cancer metastasis. This review summarizes how Bach1 controls these and other cellular and physiological and pathological processes.

Analysis of COMT Val158Met polymorphisms and methylation in Chinese male schizophrenia patients with homicidal behavior.

Schizophrenia is a severe mental disorder, and its mechanisms have not been fully elucidated. A functional single nucleotide polymorphism (SNP) present in the catechol-O-methyltransferase (COMT) gene, Val158Met (rs4680) (Chr22: 19,963,498), is possibly related to the violent behavior of schizophrenia patients. However, the specific variant that causes violent behavior is still unknown.