NEK8 promotes the progression of gastric cancer by reprogramming asparagine metabolism.

Several members of the NIMA-related kinase (NEK) family have been implicated in tumor progression; however, the role and underlying mechanisms of NEK8 in gastric cancer (GC) remain unclear. This study revealed a significant upregulation of NEK8 in GC, identifying it as an independent prognostic marker in patients with GC. Consistent with these findings, NEK8 silencing substantially impeded GC aggressiveness both in vitro and in vivo, while its overexpression produced the opposite effect.

Targeting TLK2 inhibits the progression of gastric cancer by reprogramming amino acid metabolism through the mTOR/ASNS axis.

Several recent studies have suggested that TLKs are related to tumor progression. However, the function and mechanism of action of TLK2 in gastric cancer (GC) remain elusive. In this study, TLK2 was found to be significantly upregulated in patients with GC and was identified as an independent prognostic factor for GC.

Activated Pancreatic Stellate Cells Enhance the Warburg Effect to Cause the Malignant Development in Chronic Pancreatitis.

Chronic pancreatitis (CP) is a precancerous condition associated with pancreatic ductal adenocarcinoma (PDAC), but its evolutionary mechanism is unclear. Pancreatic stellate cells (PSCs) are closely related to the occurrence and development of CP and PDAC, but it is not clear whether PSCs play a key role in this "inflammation-cancer transition". Our research found that co-culture with activated PSCs promoted the proliferation, migration and invasion of normal pancreatic duct epithelial cells and pancreatic cancer cells.

Overexpression of circRNA chr7:154954255-154998784+ in cancer-associated pancreatic stellate cells promotes the growth and metastasis of pancreatic cancer by targeting the miR-4459/KIAA0513 axis.

Purpose: Circular RNAs (circRNAs) have been reported to act as important regulators in pancreatic cancer. Abnormal expression of circRNAs in pancreatic cancer cells (PCCs) can promote the development of pancreatic cancer; however, the role of circRNAs in cancer-associated pancreatic stellate cells (CaPSCs) remains unclear.

Patients And Methods: In this study, we isolated CaPSCs from pancreatic cancer tissues from 5 pancreatic cancer patients and NaPSCs from normal pancreatic tissue from 5 patients with benign pancreatic disease.

A modified method for isolating human quiescent pancreatic stellate cells.

Background: This study explored a simple, high-yield method for isolating quiescent human pancreatic stellate cells (PSCs) to provide sufficient and reliable raw materials for PSC-related studies.

Materials And Methods: Single-cell suspensions were prepared from normal human pancreatic tissue specimens using the gentleMACS tissue processor, which enhanced the yield and viability of the suspensions. Percoll density gradient centrifugation was then performed to isolate quiescent normal PSCs (NPSCs).

Upregulated FFAR4 correlates with the epithelial-mesenchymal transition and an unfavorable prognosis in human cholangiocarcinoma.

Background: Free fatty acid receptor 4 (FFAR4) is associated with the epithelial mesenchymal transition (EMT) and is involved in the progression of several types of cancer. However, the role of FFAR4 in cholangiocarcinoma (CCA) remains unclear.

Objective: The present study evaluated the diagnosis and prognosis of CCA using FFAR4 as a biomarker.

Circular RNA Signature Predicts Gemcitabine Resistance of Pancreatic Ductal Adenocarcinoma.

Gemcitabine resistance is currently the main problem of chemotherapy for advanced pancreatic cancer patients. The resistance is thought to be caused by altered drug metabolism or reduced apoptosis of cancer cells. However, the underlying mechanism of Gemcitabine resistance in pancreatic cancer remains unclear.

The BET inhibitor I-BET762 inhibits pancreatic ductal adenocarcinoma cell proliferation and enhances the therapeutic effect of gemcitabine.

As one of the most fatal malignancies, pancreatic ductal adenocarcinoma (PDAC) has significant resistance to the currently available treatment approaches. Gemcitabine, the standard chemotherapeutic agent for locally advanced and metastatic PDAC, has limited efficacy, which is attributed to innate/acquired resistance and the activation of prosurvival pathways. Here, we investigated the in vitro efficacy of I-BET762, an inhibitor of the bromodomain and extraterminal (BET) family of proteins, in treating PDAC cell lines alone and in combination with gemcitabine (GEM).