Novel histone modifications and liver cancer: emerging frontiers in epigenetic regulation.

Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related death worldwide, and its onset and progression are closely associated with epigenetic modifications, particularly post-translational modifications of histones (HPTMs). In recent years, advances in mass spectrometry (MS) have revealed a series of novel HPTMs, including succinylation (Ksuc), citrullination (Kcit), butyrylation (Kbhb), lactylation (Kla), crotonylation (Kcr), and 2-hydroxyisobutyrylation (Khib). These modifications not only expand the histone code but also play significant roles in key carcinogenic processes such as tumor proliferation, metastasis, and metabolic reprogramming in HCC.

Dependence on the MUC1-C Oncoprotein in Classic, Variant, and Non-neuroendocrine Small Cell Lung Cancer.

Unlabelled: Small cell lung cancer (SCLC) is a recalcitrant malignancy defined by subtypes on the basis of differential expression of the ASCL1, NEUROD1, and POU2F3 transcription factors. The MUC1-C protein is activated in pulmonary epithelial cells by exposure to environmental carcinogens and promotes oncogenesis; however, there is no known association between MUC1-C and SCLC. We report that MUC1-C is expressed in classic neuroendocrine (NE) SCLC-A, variant NE SCLC-N and non-NE SCLC-P cells and activates the MYC pathway in these subtypes.

[Effects of chemical fertilizer reduction combined with humic acid bio-fertilizer on soil biological properties and dry matter mass of maize.].

A reduction of chemical fertilizers and improving fertilizer utilization rate are important for ensuring a balance between plant growth and minimizing the degradation of the black soil. We conducted a 2-year pot experiment with four treatments during 2019 and 2020, including T: no fertilizer, T: conventional use of chemical fertilizer, T: 15% reduction of the chemical fertilizer combined with 400 kg·hm of humic acid bio-fertilizer (HABF), and T: 30% reduction of the chemical fertilizer combined with 600 kg·hm of HABF, to examine the effect of reduction rates of chemical fertilizers combined with the HABF on soil microbial abundance, enzyme activity and nutrient content in maize cultivation. The results showed that the application of HABF significantly increased the abundance of soil bacteria and fungi, with the number of microbial colonies being positively correlated with the amount of HABF.

Diagnostic and Prognostic Values of KRAS Mutations on EUS-FNA Specimens and Circulating Tumor DNA in Patients With Pancreatic Cancer.

Introduction: The ability of carbohydrate antigen 19-9 (CA19-9) to differentiate pancreatic cancer from other benign pancreatic lesions is unsatisfactory. This study explored the diagnostic value of KRAS gene mutations and plasma circulating tumor DNA (ctDNA) in patients with pancreatic cancer.

Methods: The prospective cohort study comprised 149 consecutive patients with solid pancreatic lesions who underwent endoscopic ultrasound-guided fine-needle aspiration (EUS-FNA).

Targeted intervention of eIF4A1 inhibits EMT and metastasis of pancreatic cancer cells via c-MYC/miR-9 signaling.

Background: Owing to the lack of effective treatment options, early metastasis remains the major cause of pancreatic ductal adenocarcinoma (PDAC) recurrence and mortality. However, the molecular mechanism of early metastasis is largely unknown. We characterized the function of eukaryotic translation initiation factors (eIFs) in epithelial-mesenchymal-transition (EMT) and metastasis in pancreatic cancer cells to investigate whether eIFs and downstream c-MYC affect EMT and metastasis by joint interference.

MUC1-C dictates neuroendocrine lineage specification in pancreatic ductal adenocarcinomas.

Pancreatic ductal adenocarcinomas (PDAC) and poorly differentiated pancreatic neuroendocrine (NE) carcinomas are KRAS mutant malignancies with a potential common cell of origin. PDAC ductal, but not NE, lineage traits have been associated with cell-intrinsic activation of interferon (IFN) pathways. The present studies demonstrate that the MUC1 C-terminal subunit (MUC1-C), which evolved to protect mammalian epithelia from loss of homeostasis, is aberrantly overexpressed in KRAS mutant PDAC tumors and cell lines.

Targeting eIF4A using rocaglate CR‑1‑31B sensitizes gallbladder cancer cells to TRAIL‑mediated apoptosis through the translational downregulation of c‑FLIP.

Induction of the apoptosis of tumor cells is a promising therapeutic approach for the treatment of cancer. Tumor necrosis factor‑related apoptosis‑inducing ligand (TRAIL) is a novel type of anticancer drug. However, gallbladder cancer cells (GBC) exhibit strong resistance to TRAIL.

[Finite element analysis of male lower urinary tract based on the collodion slice images].

Males typically have high rates of morbidity of primary bladder neck obstruction, while the existing urodynamic examination is invasive and more likely to cause false diagnosis. To build a non-invasive biomechanical detecting system for the male lower urinary tract, a finite element model for male lower urinary tract based on the collodion slice images of normal male lower urinary tract was constructed, and the fluid-structure interaction of the lower urinary tract was simulated based on the real urination environment. The finite element model of the lower urinary tract was validated by comparing the clinical experiment data with the simulation result.

Simvastatin augments activation of liver regeneration through attenuating transforming growth factor-β1 induced-apoptosis in obstructive jaundice rats.

Obstructive jaundice, owing to biliary obstruction, has been illustrated to trigger various biochemical, histological and immunological changes, leading to liver damage or even failure. The detailed molecular mechanism of simvastatin (Sim) involvement in liver regeneration during obstructive jaundice progression remains poorly elucidated. In the present study, an acute obstructive jaundice rat model was established by ligation and division of common bile duct, which was used to investigate the effects of Sim as a hepatoprotective treatment.

Prohibitin overexpression predicts poor prognosis and promotes cell proliferation and invasion through ERK pathway activation in gallbladder cancer.

Background: Prohibitin (PHB), a pleiotropic protein overexpressed in several tumor types, has been implicated in the regulation of cell proliferation, invasive migration and survival. However, PHB expression and its biological function in gallbladder cancer (GBC) remain largely unknown.

Methods: PHB and p-ERK protein expressions were determined in human GBC tissues by immunohistochemistry (IHC).

Overexpression of uncoupling protein 2 inhibits the high glucose-induced apoptosis of human umbilical vein endothelial cells.

Ectopic apoptosis of vascular cells plays a critical role in the early stage development of diabetic retinopathy (DR). Uncoupling protein 2 (UCP2) is a mitochondrial modulator which protects against endothelial dysfunction. However, the role which UCP2 plays in endothelial apoptosis and its association with DR was unclear.

Rocaglamide overcomes tumor necrosis factor-related apoptosis-inducing ligand resistance in hepatocellular carcinoma cells by attenuating the inhibition of caspase-8 through cellular FLICE-like-inhibitory protein downregulation.

The enhancement of apoptosis is a therapeutic strategy used in the treatment of cancer. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a promising antitumor agent. However, hepatocellular carcinoma (HCC) cells exhibit marked resistance to the induction of cell death by TRAIL.

Neuropilin 1 expression in human aortas, coronaries and the main bypass grafts.

Objectives: Development of intimal hyperplasia (IH) is the main pathology underlying graft failure following coronary artery bypass graft surgeries for ischaemic heart diseases, especially for great saphenous vein grafts which have a lower patency rate than internal mammary arteries. Neuropilin 1 (NRP1), which is a co-receptor for vascular endothelial growth factor found in vascular endothelial and smooth muscle cells, affects the development of IH. We examined the difference in NRP1 expression and distribution in human coronaries, aortas, mammary arteries and saphenous veins to detect a possible relation to their susceptibility to IH.

Targeting the prohibitin scaffold-CRAF kinase interaction in RAS-ERK-driven pancreatic ductal adenocarcinoma.

Background: Robust ERK1/2 activity, which frequently results from KRAS mutation, invariably occurs in pancreatic ductal adenocarcinoma (PDAC). However, direct interference of KRAS signaling has not led to clinically successful drugs. Correct localization of RAF is regulated by the scaffold protein prohibitin (PHB) that ensures the spatial organization between RAS and RAF in plasma membranes, thus leading to activation of downstream effectors.