Downregulated KLF4, induced by m6A modification, aggravates intestinal barrier dysfunction in inflammatory bowel disease.

Background: Krüppel-like factor 4 (KLF4), a transcription factor, is involved in various biological processes. However, the role of KLF4 in regulating the intestinal epithelial barrier (IEB) in inflammatory bowel disease (IBD) and its mechanism have not been extensively studied.

Methods: KLF4 expression in IBD patients and colitis mice was analyzed using Gene Expression Omnibus(GEO) database, immunohistochemistry (IHC) and Western blot.

Vitamin B6 ameliorates acute pancreatitis by suppressing the caspase3 signaling pathway.

Background: Acute pancreatitis (AP) is a prevalent exocrine inflammatory disorder of the pancreas characterized by pancreatic inflammation and injury to acinar cells. Vitamin B6 (VB6) is a vital nutrient that plays a significant role in preserving human health and has anti-inflammatory and anti-apoptotic effects.

Methods: This study aimed to explore the potential pancreatic protective effects of VB6 in mitigating pancreatic inflammation and apoptosis induced by taurocholate sodium (TLCS) in an AP model and to assess the underlying mechanism of action.

CAFs secrete CXCL12 to accelerate the progression and cisplatin resistance of colorectal cancer through promoting M2 polarization of macrophages.

The purpose of this study was to investigate the effect of the interaction between tumor-associated fibroblasts (CAFs) and macrophage polarization on colorectal cancer (CRC) progression. Clinical tissue samples of CRC and health volunteers were collected to isolate normal fibroblasts (NFs) and CAFs. LoVo, HCT116, or THP-1 cells were co-cultured with NFs or CAFs.

Cancer-associated fibroblasts-derived exosomes from chemoresistant patients regulate cisplatin resistance and angiogenesis by delivering VEGFA in colorectal cancer.

The purpose of this study was to investigate the effect of chemoresistant cancer-associated fibroblasts (R-CAFs) against cisplatin (DDP) on colorectal cancer (CRC) progression. First, clinical tissue samples of chemoresistant or chemosensitive CRC patients were collected to isolate R-CAFs or chemosensitive CAFs (S-CAFs), respectively. HT29 cells or HUVECs were co-cultured with R-CAFs by transwell device.

Knockdown of membrane-bound complement regulatory proteins suppresses colon cancer growth in mice through inducing tumor cell apoptosis.

CD46, CD55 and CD59 are membrane-bound complement regulatory proteins (mCRPs) and highly expressed in many tumor tissues. Our analysis by RNA sequencing and qRT-PCR revealed that the expression of mCRPs was significantly elevated in cancer tissues of 15 patients with colon cancer. To further investigate the role of mCRPs in the development of colon cancer, we suppressed the expression of mCRPs by CD46-shRNA, CD55-shRNA and CD59-shRNA in colon cancer cell lines, SW620 and HT-29 cells.

ALKBH5-mediated mA demethylation of KCNK15-AS1 inhibits pancreatic cancer progression via regulating KCNK15 and PTEN/AKT signaling.

Long noncoding RNAs (lncRNAs) are regarded as crucial regulators in tumor progression. Potassium two pore domain channel subfamily K member 15 and WISP2 antisense RNA 1 (KCNK15-AS1) has been confirmed to inhibit the migration and invasion of pancreatic cancer (PC) cells. However, its downstream mechanism and effect on other cellular functions in PC remain unknown.