Silencing of KIAA1429, a N6-methyladenine methyltransferase, inhibits the progression of colon adenocarcinoma via blocking the hypoxia-inducible factor 1 signalling pathway.

KIAA1429 is an important 'writer' of the N6-methyladenine (mA) modification, which is involved in tumour progression. This study was conducted to explore the mechanism of action of KIAA1429 in colon adenocarcinoma (COAD). KIAA1429-silenced COAD cell and xenograft tumour models were constructed, and the function of KIAA1429 was explored through a series of in vivo and in vitro assays.

Protopine alleviates lipopolysaccharide-triggered intestinal epithelial cell injury through retarding the NLRP3 and NF-κB signaling pathways to reduce inflammation and oxidative stress.

Background: Inflammatory bowel disease (IBD) is a common chronic intestinal disease. Protopine isolated from different plants has been investigated to understand its special functions on varied diseases. However, the regulatory effects of protopine on the progression of IBD remain unclear.

Upregulation of lncRNA HITT promotes cell apoptosis by suppressing the maturation of miR-602 in gastric cancer.

It has been reported that HITT can inhibit colon cancer. However, the role of HITT in gastric cancer (GC) is unknown. Our preliminary sequencing data revealed the altered expression of HITT in GC and its close correlation with miR-602, suggesting the involvement of HITT and its potential interaction with miR-602 in GC.

Forkhead box A2 transcriptionally activates hsa-let-7 g to inhibit hypoxia-induced epithelial-mesenchymal transition by targeting c14orf28 in colorectal cancer.

Background And Study Aims: This study aimed to investigate the effect of Forkhead Box A2 (FOXA2) on migration, invasion, and epithelial-mesenchymal transition (EMT) of colorectal cancer (CRC) cells in hypoxia and explore its related molecular mechanisms.

Patients And Methods: A cellular hypoxia model was established, and the FOXA2 overexpression vector was transfected into SW480 and HCT116 cells. Cell apoptosis, migration, and invasion were examined by flow cytometry, scratch test, and transwell-invasion assay.

Expression of serum autophagy-related protein P62 in patients with severe pancreatitis and its correlation with prognosis.

Objective: This study was designed to investigate the expression of serum autophagy-related protein P62 in patients with severe acute pancreatitis (AP) and its correlation with prognosis.

Methods: Eighty patients with AP treated in the First Affiliated Hospital of Gannan Medical University from January 2020 to January 2021 were enrolled as study subjects in this retrospective analysis, and they were placed into the mild AP group (n=52) or the severe AP group (n=28). According to clinical outcomes, these 80 patients were divided into a good prognosis group (GP group, n=51, surviving without serious complications such as organ failure) and a poor prognosis group (PP group, n=29, death or developing organ failure).

MT1G inhibits the growth and epithelial-mesenchymal transition of gastric cancer cells by regulating the PI3K/AKT signaling pathway.

Gastric carcinoma (GC) is a malignant tumor that has high mortality and morbidity worldwide. Although many efforts have been focused on the development and progression of GC, the underlying functional regulatory mechanism of GC needs more clarification. Metallothionein 1G (MT1G) is a member of the metallothionein family (MTs), and hypermethylation of MT1G occurred in a variety of cancers, including gastric cancer.

SYNPO2 suppresses hypoxia-induced proliferation and migration of colorectal cancer cells by regulating YAP-KLF5 axis.

Colorectal cancer (CRC) is one of the most common tumors that has a high incidence worldwide. Targeted therapy for CRC has received much attention recently. It is still necessary to develop novel and promising therapeutic targets to improve the prognosis.

Neuronal pentraxin II (NPTX2) hypermethylation promotes cell proliferation but inhibits cell cycle arrest and apoptosis in gastric cancer cells by suppressing the p53 signaling pathway.

Gastric cancer is a considerable health burden worldwide. DNA methylation, a major epigenetic phenomenon, is closely related to the pathogenesis of cancer. Neuronal pentraxin II (NPTX2) has been found to be hypermethylated in several cancers such as glioblastoma and pancreatic cancer.

A bioinformatic and mechanistic study elicits the antifibrotic effect of ursolic acid through the attenuation of oxidative stress with the involvement of ERK, PI3K/Akt, and p38 MAPK signaling pathways in human hepatic stellate cells and rat liver.

NADPH oxidases (NOXs) are a predominant mediator of redox homeostasis in hepatic stellate cells (HSCs), and oxidative stress plays an important role in the pathogenesis of liver fibrosis. Ursolic acid (UA) is a pentacyclic triterpenoid with various pharmacological activities, but the molecular targets and underlying mechanisms for its antifibrotic effect in the liver remain elusive. This study aimed to computationally predict the molecular interactome and mechanistically investigate the antifibrotic effect of UA on oxidative stress, with a focus on NOX4 activity and cross-linked signaling pathways in human HSCs and rat liver.

[Effect of ursolic acid on proliferation and apoptosis of hepatic stellate cells in vitro].

Objective: To investigate the effect of ursolic acid on proliferation and apoptosis of hepatic stellate cells (HSC) in vitro and explore the mechanisms of apoptosis of HSC induced by ursolic acid by studying the expressions of apoptosis-regulating proteins Bcl-2, Bax and Caspase 3 in HSC.

Methods: Hepatic stellate cells HSC-T6 and hepatocytes L02 were incubated with different concentrations of ursolic acid (25, 50, 75, 100, 125 and 150 micromol/L) for 24 h, 48 h and 72 h. The effect of ursolic acid on the cell proliferation was studied by methyl thiazolyl tetrazolium (MTT) colorimetric assay.