Hypoxia-induced autophagy in pancreatic cancer counteracts the cytotoxicity of CD8 T cells by inhibiting the expression of MHC-I.

The hypoxic microenvironment is an essential feature of solid tumors. Autophagy has been controversial in its role in immune regulation. This project aims to elucidate the impact of autophagy in pancreatic cancer (PC) under specific conditions (hypoxia) on CD8 T cells and the regulatory mechanisms behind it.

ITGB4/BNIP3 Activates Autophagy and Reduces MHC-I Expression to Mediate Tumour Immune Escape in Pancreatic Cancer Cell Lines.

This study attempted to identify the relevant pathways involved in autophagy activation of pancreatic cancer and explore the mechanisms underlying immune evasion. Western blot (WB) was used to detect the expression of ITGB4, BNIP3, autophagy-related proteins and MHC-I. Co-immunoprecipitation (Co-IP) was used to verify the binding mode of ITGB4 and BNIP3.

HIF-3α Facilitates the Proliferation and Migration in Pancreatic Cancer by Inhibiting Autophagy Through Downregulating TP53INP2.

Pancreatic cancer is a highly aggressive malignant tumor, often diagnosed late, leading to a poor prognosis and extremely high mortality rates. In recent years, the role of cellular autophagy in tumors has become increasingly prominent, gradually becoming an important target for malignant tumors. HIF-3α is a member of HIF family with potential oncogenic function.

MiR-93-5P Represses the Gluconeogenesis of Hepatocellular Carcinoma while Boosting Its Glycolysis and Malignant Progression by Suppressing PCK1.

Herein, we explored effects of miR-93-5p and gluconeogenic rate-limiting enzyme PCK1 on HCC cells. Bioinformatics analysis and cell experiments confirmed that, compared with expression in normal tissue and cells, miR-93-5p in HCC was abnormally upregulated while PCK1 expression was remarkably downregulated. PCK1 overexpression repressed proliferation, migration, and invasion of HCC cells, and blocked cell cycle in G0/G1 phase.

Reduced triglyceride accumulation due to overactivation of farnesoid X receptor signaling contributes to impaired liver regeneration following 50% hepatectomy in extra‑cholestatic liver tissue.

The aim of the present study was to investigate the role of triglyceride metabolism in the effect of obstructive cholestasis on liver regeneration following 50% partial hepatectomy (PH). Obstructive cholestatic rat models were achieved via ligation of the common bile duct (BDL). Following comparisons between hepatic pathological alterations with patients with perihilar cholangiocarcinoma, rats in the 7 day post‑BDL group were selected as the BDL model for subsequent experiments.

Histological classification of microvascular invasion to predict prognosis in intrahepatic cholangiocarcinoma.

Similar to hepatocellular carcinoma, microvascular invasion (MVI) is also one of the most significant prognostic factors of intrahepatic cholangiocarcinoma (ICC). However, there has not been any literature that had mentioned the histologic classification of microvascular invasion in intrahepatic cholangiocarcinoma. We evaluated the significance of MVI classification in this study and analyzed the prognosis based on MVI classification.

Contrast-enhanced computed tomography plus gadolinium-ethoxybenzyl diethylenetriamine pentaacetic acid-enhanced magnetic resonance imaging for gross classification of hepatocellular carcinoma.

Accurate gross classification through imaging is critical for determination of hepatocellular carcinoma (HCC) patient prognoses and treatment strategies. The present retrospective study evaluated the utility of contrast-enhanced computed tomography (CE-CT) combined with gadolinium-ethoxybenzyl diethylenetriamine pentaacetic acid-enhanced magnetic resonance imaging (EOB-MRI) for diagnosis and classification of HCCs prior to surgery. Ninety-four surgically resected HCC nodules were classified as simple nodular (SN), SN with extranodular growth (SN-EG), confluent multinodular (CMN), or infiltrative (IF) types.

Mutation Detection of Fibroblast Growth Factor Receptor 3 for Infiltrative Hepatocellular Carcinoma by Whole-Exome Sequencing.

Background: Gene data on infiltrative hepatocellular carcinoma (iHCC) are still unknown.

Aims: This study aims to identify the gene expression signature of iHCC compared with single nodular (SN)-type HCC according to the gross classification.

Methods: The whole-exome sequencing was performed in six matched HCC tumor/normal pairs (three infiltrative type and three single nodular type) from six patients who received curative hepatectomy.