AC074117.1/miR-193a-3p axis regulates the malignant progression of uterine corpus endometrial carcinoma via the m6A-related gene ALKBH5.

Uterine corpus endometrial carcinoma (UCEC) is one of the most common gynecological malignancies, with an annually increasing incidence and a poor prognosis. lncRNAs and microRNAs regulate the progression of UCEC through ceRNA networks. Additionally, m6A modification plays various roles in UCEC, and abnormal regulation of it can directly affect tumor progression.

Evaluation of the toxoplasma Urm1 gene deletion mutant (PruΔUrm1) as a promising vaccine candidate against toxoplasmosis in mice.

Toxoplasmosis is a significant zoonotic disease that poses a serious threat to both human and animal health. Despite ongoing research, developing an effective vaccine for toxoplasmosis remains a challenge. In this study, we evaluated the vaccine potential of the Toxoplasma Urm1 gene deletion mutant (PruΔUrm1) by assessing its pathogenicity and protective efficacy in mice.

Exosomal miR-146a-5p Derived from HSCs Accelerates Sepsis-induced Liver Injury by Suppressing KLF-4.

This study aimed to investigate whether and how lipopolysaccharide (LPS) activated hepatic stellate cells (HSCs) regulate macrophage activity and to explore the impact of microRNAs (miRNAs) in exosomes from HSCs on this process. Mice subjected to LPS or cecal ligation and puncture (CLP) were used to explore sepsis-induced liver injury. Liver injury was evaluated using HE staining, and alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels were measured.

DOK1 facilitates the advancement of ccRCC.

Renal cell carcinoma (RCC) is one of the most common human cancers. Clear cell renal cell carcinoma (ccRCC) is a major subtype of RCC. However, the molecular mechanisms underlying ccRCC oncogenesis require further investigation.

Can the return of rural labor improve the physical health of left-behind parents-evidence from rural China.

Objectively In objective terms, the return of rural labor force shortens the spatial distance with parents, leading to changes in caregiving support, emotional support, and financial support for parents, thereby affecting the health status of parents. This article, using data from the Chinese Family Panel Studies, analyzes the characteristics of the health status of parents with and without returning migrant children. By employing multiple linear regression models, PSM models, and IV-2SLS methods to address endogeneity bias, the study preliminarily explores the impact of rural labor force return on parental health.

mA demethylation of FOSL1 mRNA protects hepatoma cells against necrosis under glucose deprivation.

Stress-adaptive mechanisms enabling cancer cells to survive under glucose deprivation remain elusive. N-methyladenosine (mA) modification plays important roles in determining cancer cell fate and cellular stress response to nutrient deficiency. However, whether mA modification functions in the regulation of cancer cell survival under glucose deprivation is unknown.

Hyperthermia and associated changes in membrane fluidity potentiate P2X7 activation to promote tumor cell death.

Extracellular ATP (eATP) accumulation within the tumor microenvironment (TME) has the potential to activate purinergic signaling. The eATP evoked signaling effects bolster antitumor immune responses while exerting direct cytotoxicity on tumor cells and vascular endothelial cells, mediated at least in part through P2X7 receptors. Approaches to augment purinergic signaling in TME e.

P2X7 integrates PI3K/AKT and AMPK-PRAS40-mTOR signaling pathways to mediate tumor cell death.

Background: Extracellular adenosine triphosphate (ATP) functions as a novel danger signal that boosts antitumor immunity and can also directly kill tumor cells. We have previously reported that chronic exposure of tumor cells to ATP provokes P2X7-mediated tumor cell death, by as yet incompletely defined molecular mechanisms.

Methodology/principal Findings: Here, we show that acute exposure of tumor cells to ATP results in rapid cytotoxic effects impacting several aspects of cell growth/survival, leading to inhibition of tumor growth in vitro and in vivo.

CD39 modulates hematopoietic stem cell recruitment and promotes liver regeneration in mice and humans after partial hepatectomy.

Objective: To study molecular mechanisms involved in hematopoietic stem cell (HSC) mobilization after liver resection and determine impacts on liver regeneration.

Background: Extracellular nucleotide-mediated cell signaling has been shown to boost liver regeneration. Ectonucleotidases of the CD39 family are expressed by bone marrow-derived cells, and purinergic mechanisms might also impact mobilization and functions of HSC after liver injury.

Percutaneous transhepatic variceal embolization combined with endoscopic ligation for the prevention of variceal rebleeding.

Objective: To compare the efficiency of percutaneous transhepatic variceal embolization (PTVE) plus endoscopic variceal ligation (EVL) with EVL alone in the treatment of esophageal variceal bleeding.

Methods: Cirrhotic patients with recent esophageal variceal bleeding from January 2007 to December 2011 were collected and assigned to PTVE + EVL (N = 41) or EVL (N = 47) groups. We performed chart reviews and prospective follow-up to determine variceal rebleeding, recurrence of varices and survival.

Disordered purinergic signaling and abnormal cellular metabolism are associated with development of liver cancer in Cd39/ENTPD1 null mice.

Unlabelled: Liver cancer is associated with chronic inflammation, which is linked to immune dysregulation, disordered metabolism, and aberrant cell proliferation. Nucleoside triphosphate diphosphohydrolase-1; (CD39/ENTPD1) is an ectonucleotidase that regulates extracellular nucleotide/nucleoside concentrations by scavenging nucleotides to ultimately generate adenosine. These properties inhibit antitumor immune responses and promote angiogenesis, being permissive for the growth of transplanted tumors.

Vascular CD39/ENTPD1 directly promotes tumor cell growth by scavenging extracellular adenosine triphosphate.

Extracellular adenosine triphosphate (ATP) is known to boost immune responses in the tumor microenvironment but might also contribute directly to cancer cell death. CD39/ENTPD1 is the dominant ectonucleotidase expressed by endothelial cells and regulatory T cells and catalyzes the sequential hydrolysis of ATP to AMP that is further degraded to adenosine by CD73/ecto-5'-nucleotidase. We have previously shown that deletion of Cd39 results in decreased growth of transplanted tumors in mice, as a result of both defective angiogenesis and heightened innate immune responses (secondary to loss of adenosinergic immune suppression).