Hsa_circ_0007590/PTBP1 complex reprograms glucose metabolism by reducing the stability of mA-modified PTEN mRNA in pancreatic ductal adenocarcinoma.

The role of circular RNAs (circRNAs) in glucose metabolism in pancreatic duct adenocarcinoma (PDAC) remains elusive. Through RNA sequencing of cells cultured under conditions of glucose deprivation, we identified hsa_circ_0007590. Sanger sequencing and RNase R and Act D treatments were performed to confirm the circular RNA features of hsa_circ_0007590.

Comprehensive Analysis of PPMs in Pancreatic Adenocarcinoma Indicates the Value of in the Tumor Microenvironment.

Early metastasis and resistance to traditional therapy are responsible for the poor prognosis of pancreatic adenocarcinoma patients. Metal-dependent protein phosphatases (PPMs) have been proven to play a crucial role in the initiation and progression of various tumors. Nevertheless, the expression and function of distinct PPMs in pancreatic adenocarcinoma have not been fully elucidated.

METTL16 predicts a favorable outcome and primes antitumor immunity in pancreatic ductal adenocarcinoma.

Pancreatic carcinogenesis is a complicated and multi-step process. It is substantially assisted by N6-methyladenosine (mA) RNA modification, especially when mutations of driver genes (KRAS, TP53, CDKN2A, and SMAD4) occur. However, the underlying mechanism remains obscure.

CircMYOF triggers progression and facilitates glycolysis via the VEGFA/PI3K/AKT axis by absorbing miR-4739 in pancreatic ductal adenocarcinoma.

Emerging evidence has demonstrated that circular RNAs (circRNAs) take part in the initiation and development of pancreatic ductal adenocarcinoma (PDA), a deadly neoplasm with an extremely low 5-year survival rate. Reprogrammed glucose metabolism is a key feature of tumour development, including PDA. In this research, we evaluated the role of circRNAs in reprogrammed glucose metabolism in PDA.

SLC45A4 promotes glycolysis and prevents AMPK/ULK1-induced autophagy in TP53 mutant pancreatic ductal adenocarcinoma.

Background: Somatic mutations of the TP53 gene occur frequently in pancreatic ductal adenocarcinoma (PDA). Solute carrier family 45 member A4 (SLC45A4) is a H -dependent sugar cotransporter. The role of SLC45A4 in PDA, especially in TP53 mutant PDA, remains poorly understood.

LncRNA PVT1 triggers Cyto-protective autophagy and promotes pancreatic ductal adenocarcinoma development via the miR-20a-5p/ULK1 Axis.

Background: Defective autophagy is thought to contribute to the pathogenesis of many diseases, including cancer. Human plasmacytoma variant translocation 1 (PVT1) is an oncogenic long non-coding RNA that has been identified as a prognostic biomarker in pancreatic ductal adenocarcinoma, but how PVT1 operates in the regulation of autophagy in pancreatic ductal adenocarcinoma (PDA) is unclear.

Methods: PVT1 expression level was detected by quantitative real-time polymerase chain reaction (qRT-PCR) and hybridization in situ (ISH).

The novel long intergenic noncoding RNA UCC promotes colorectal cancer progression by sponging miR-143.

The human genome contains thousands of long intergenic noncoding RNAs (lincRNAs). However, the functional roles of these transcripts and the mechanisms responsible for their deregulation in colorectal cancer (CRC) remain elusive. A novel lincRNA termed upregulated in CRC (UCC) was found to be highly expressed in human CRC tissues and cell lines.

Hepatic perivascular epithelioid cell neoplasm: A clinical and pathological experience in diagnosis and treatment.

Hepatic perivascular epithelioid cell neoplasm (PEComa) is a rare type of neoplasm derived from mesenchymal tumors that is often misdiagnosed as hepatocellular carcinoma (HCC), hepatic hemangioma or other liver malignancies. The clinical and histological characteristics of PEComa have yet to be fully documented. To optimize the diagnosis and treatment of the disease, a retrospective analysis was performed to investigate the clinicopathological characteristics of 7 patients diagnosed with hepatic PEComa in the Sun Yat-Sen Memorial Hospital between January 2004 and December 2015.

MiR-143 Targeting TAK1 Attenuates Pancreatic Ductal Adenocarcinoma Progression via MAPK and NF-κB Pathway In Vitro.

Background: Transforming growth factor (TGF)-β-activated kinase 1 (TAK1) is one of the major regulators of inflammation-induced cancer cell growth and progression. MiR-143 dysregulation is a common event in a variety of human diseases including pancreatic ductal adenocarcinoma (PDA).

Aims: To identify the interaction between TAK1 and miR-143 in PDA.