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.

Lysyl hydroxylase LH1 promotes confined migration and metastasis of cancer cells by stabilizing Septin2 to enhance actin network.

Background: Excessive extracellular matrix deposition and increased stiffness are typical features of solid tumors such as hepatocellular carcinoma (HCC) and pancreatic ductal adenocarcinoma (PDAC). These conditions create confined spaces for tumor cell migration and metastasis. The regulatory mechanism of confined migration remains unclear.

USP9X-mediated NRP1 deubiquitination promotes liver fibrosis by activating hepatic stellate cells.

Liver fibrosis is a complex fibrotic process that develops early in the course of cirrhosis and is caused by chronic liver damage. The activation of hepatic stellate cells is primarily responsible for the fibrosis process. Studies show that NRP1 influences HSC motility and migration.

Rab31 promotes activation of hepatic stellate cells by accelerating TGF-β receptor II complex endocytosis.

Background & Aims: Hepatic stellate cells activation is the key process of liver fibrosis, revealing the molecular mechanism of which is helpful to provide an effective target for inhibiting liver fibrosis. Rab31, a small GTPase, regulates the specificity of intracellular vesicular transport system, and is crucial for signal transduction. However, whether Rab31 is involved in hepatic stellate cells activation is unknown.

Epigenetic silencing of GCH1promotes hepatocellular carcinoma growth by activating superoxide anion-mediated ASK1/p38 signaling via inhibiting tetrahydrobiopterin de novo biosynthesis.

Metabolic reprogramming is a hallmark of cancer, including hepatocellular carcinoma (HCC). However, its role in HCC remains to be elucidated. Herein, we identified GTP cyclohydrolase 1 (GCH1), the first rate-limiting enzyme in tetrahydrobiopterin (BH4) de novo biosynthesis, as a novel metabolic regulator of HCC.

Ubiquitin-specific protease 2a promotes hepatocellular carcinoma progression via deubiquitination and stabilization of RAB1A.

Purpose: Deubiquitination, the inverse process of ubiquitination, is catalyzed by deubiquitinases (DUBs) that remove ubiquitin from target proteins and subsequently prevent their degradation by proteasomes. Previously, deubiquitination has been found to be involved in hepatocellular carcinoma (HCC) progression. As yet, however, little is known about the exact role of deubiquitination in the development and/or progression of this type of cancer.

Cholesterol impairs hepatocyte lysosomal function causing M1 polarization of macrophages via exosomal miR-122-5p.

Nonalcoholic steatohepatitis (NASH) is a major threat to health worldwide. Lipotoxicity and macrophage-mediated inflammation play key roles in the pathogenesis of NASH. In this study, we found that individuals with higher serum LDL-C levels have a higher prevalence of nonalcoholic fatty liver disease (NAFLD) and elevated levels of glutamic-pyruvic transaminase, glutamic-oxalacetic transaminase and alkaline phosphatase.

Cholesterol attenuated the progression of DEN-induced hepatocellular carcinoma via inhibiting SCAP mediated fatty acid de novo synthesis.

Worldwide, hepatocellular carcinoma (HCC) remains a top instigator of cancer mortality. Previous clinical studies have revealed that low serum cholesterol predicts a poor outcome in HCC patients, but the potential role of cholesterol in the progression of HCC remains controversial. In the present study,we tested the influence of cholesterol on the progression of DEN-induced HCC by feeding mice with a high cholesterol diet (HCD) and by depriving cholesterol with atorvastatin, a widely used inhibitor of the mevalonate pathway.

Ubiquitin-specific protease 4 promotes metastasis of hepatocellular carcinoma by increasing TGF-β signaling-induced epithelial-mesenchymal transition.

Invasion and metastasis are the main cause of recurrence and death in advanced hepatocellular carcinoma (HCC). Revealing the mechanisms of HCC metastasis is important for developing new therapeutic approaches and reducing patient mortality. Ubiquitin specific protease 4 (USP4), is involved in tumorigenesis by deubiquitinating some important oncogenic proteins and impacting their degradation.

Inhibition of DACH1 activity by short hairpin RNA represses cell proliferation and tumor invasion in pancreatic cancer.

Cancer of the pancreas is one of the most lethal diseases worldwide. Better understanding of the molecular mechanisms involved in tumorigenesis is of great consequence to elevate the survival rate. Human Dachshund homologue 1 (DACH1) plays a controversial role in human malignancy progression with its expression being altered in a variety of cancers.

Protocadherin-10 acts as a tumor suppressor gene, and is frequently downregulated by promoter methylation in pancreatic cancer cells.

Protocadherin-10 (PCDH10), a member of non-clustered protocadherin family which plays important roles in calcium-dependent cell-cell signal transduction and adhesion. PCDH10 functions as a tumor suppressor gene and its expression is downregulated by promoter methylation in many malignances. In the present study, we explored PCDH10 expression and promoter methylation status, and its biological effects in pancreatic cancer cells, and furthermore, we explored the mechanism of PCDH10 preliminary in pancreatic cancer cells.

[Protocadherin 10 (PCDH10) inhibits the proliferation, invasion and migration ability of BXPC-3 pancreatic cancer cells].

Objective: To explore the expression and biological function of protocadherin 10 (PCDH10) in pancreatic cancer cells.

Methods: Reverse transcription PCR (RT-PCR) was used to detect the expression of PCDH10 in CAPAN-1, PANC-1, ASPC-1, BXPC-3 pancreatic cancer cells and the HPDE6-C7 normal human pancreatic ductal epithelial cells. Recombinant plasmid pcDNA3.