BICC1 drives pancreatic cancer stemness and chemoresistance by facilitating tryptophan metabolism.

Pancreatic adenocarcinoma is the fourth leading cause of malignancy-related deaths, with rapid development of drug resistance driven by pancreatic cancer stem cells. However, the mechanisms sustaining stemness and chemotherapy resistance in pancreatic ductal adenocarcinoma (PDAC) remain unclear. Here, we demonstrate that Bicaudal C homolog 1 (BICC1), an RNA binding protein regulating numerous cytoplasmic mRNAs, facilitates chemoresistance and stemness in PDAC.

Tumor-derived interleukin 35 mediates the dissemination of gemcitabine resistance in pancreatic adenocarcinoma.

Rapid development of drug resistance after chemotherapy is a major cause of treatment failure in individuals with pancreatic ductal adenocarcinoma (PDAC). In this study, we illustrate that tumor-derived interleukin 35 (IL-35) mediates the accelerated resistance of PDAC to gemcitabine (GEM). We observe that GEM resistance can spread from GEM-resistant PDAC cells to GEM-sensitive cells, and that IL-35 is responsible for the propagation of chemoresistance, which is supported by sequencing and experimental data.

Dual-Color Lasers in Interlayer-Free Solution Processed Polymeric Bilayer Devices.

Multiwavelength organic lasers have attracted considerable interest in recent years due to the cost efficiency, wide luminescence coverage, and simple processability of organics. In this work, by simply spin coating immiscible polymeric gain media in sequence, dual-wavelength (blue-green or blue-red) amplified spontaneous emission (ASE) was achieved in bilayer devices. The blue emission, water/alcohol-soluble conjugated polyelectrolyte, poly[(9,9-bis(3'-((,-dimethyl)--ethylammonium)-propyl)-2,7-fluorene)-alt-2,7-(9,9-dioctylfluorene)]dibromide (PFN-Br), was used as the bottom layer.

BICC1 drives pancreatic cancer progression by inducing VEGF-independent angiogenesis.

VEGF inhibitors are one of the most successful antiangiogenic drugs in the treatment of many solid tumors. Nevertheless, pancreatic adenocarcinoma (PAAD) cells can reinstate tumor angiogenesis via activation of VEGF-independent pathways, thereby conferring resistance to VEGF inhibitors. Bioinformatic analysis showed that BICC1 was one of the top genes involved in the specific angiogenesis process of PAAD.

RIPK1-dependent necroptosis promotes vasculogenic mimicry formation via eIF4E in triple-negative breast cancer.

Necroptosis is a caspase-independent form of programmed cell death. Receptor interacting protein kinase 1 (RIPK1) is a key molecule in the initiation of necroptosis and the formation of the necrotic complex. Vasculogenic mimicry (VM) provides a blood supply to tumor cells that is not dependent on endothelial cells.

MIF promotes cell invasion by the LRP1-uPAR interaction in pancreatic cancer cells.

Introduction: Pancreatic ductal adenocarcinoma (PDAC) is characterized by high aggressiveness and a hypoxic tumour microenvironment. Macrophage migration inhibitory factor (MIF) is a hypoxia-related pleiotropic cytokine that plays important roles in cancer. However, its role in PDAC progression has not been fully elucidated.

The relevance between hypoxia-dependent spatial transcriptomics and the prognosis and efficacy of immunotherapy in claudin-low breast cancer.

Introduction: Hypoxia is an important characteristic of solid tumors. However, spatial transcriptomics (ST) of hypoxia-associated heterogeneity is not clear.

Methods: This study integrated Spatial Transcriptomics (ST) with immunofluorescence to demonstrate their spatial distribution in human claudin-low breast cancer MDA-MB-231 engraft.

ENO1 expression and Erk phosphorylation in PDAC and their effects on tumor cell apoptosis in a hypoxic microenvironment.

Objective: Hypoxia is an important feature of pancreatic ductal adenocarcinoma (PDAC). Previously, we found that hypoxia promotes ENO1 expression and PDAC invasion. However, the underlying molecular mechanism was remains unclear.

Genome-wide CRISPR screen identifies MTA3 as an inducer of gemcitabine resistance in pancreatic ductal adenocarcinoma.

Gemcitabine (GEM) resistance is one of the major causes of treatment failure in pancreatic ductal adenocarcinoma (PDAC) in clinic. Here, through CRISPR/Cas9 activation library screen, we found that MTA3 mediates the GEM resistance of PDAC and thus might be a potential therapeutic target for combination chemotherapy. The CRISPR library screening showed that MTA3 is the most enriched gene in the surviving GEM-treated cells, and bioinformatic and histology analysis implied its high correlation with GEM resistance.

OXCT1 Enhances Gemcitabine Resistance Through NF-κB Pathway in Pancreatic Ductal Adenocarcinoma.

Background: Pancreatic ductal adenocarcinoma (PDAC) is a type of malignant tumor with a five-year survival rate of less than 10%. Gemcitabine (GEM) is the most commonly used drug for PDAC chemotherapy. However, a vast majority of patients with PDAC develop resistance after GEM treatment.

Hypoxic microenvironment induced spatial transcriptome changes in pancreatic cancer.

Objective: Hypoxia is a significant feature of solid tumors, including pancreatic ductal adenocarcinoma (PDAC). It is associated with tumor invasion, metastasis, and drug resistance. However, the spatial distribution of hypoxia-related heterogeneity in PDAC remains unclear.

PERK-eIF2α-ERK1/2 axis drives mesenchymal-endothelial transition of cancer-associated fibroblasts in pancreatic cancer.

Pancreatic ductal adenocarcinoma (PDAC) is characterized by remarkable desmoplasia, usually driven by cancer-associated fibroblasts (CAFs), influencing patient prognosis. CAFs are a group of plastic cells responsible for tumor growth and metastasis. Fibroblasts have been reported to directly contribute to angiogenesis by undergoing mesenchymal-endothelial transition (MEndoT) after ischemic injury in the heart, brain, and hindlimbs.

Twist1 accelerates tumour vasculogenic mimicry by inhibiting Claudin15 expression in triple-negative breast cancer.

The up-regulation of EMT regulator Twist1 has been implicated in vasculogenic mimicry (VM) formation in human triple-negative breast cancer (TNBC). Twist1 targets the Claudin15 promoter in hepatocellular carcinoma cells. Claudin family members are related with TNBC.

A noble bimetal oxysulfide CuOS catalyst for highly efficient catalytic reduction of 4-nitrophenol and organic dyes.

A novel copper-vanadium bimetallic oxysulfide (CuOS) nanoparticle catalyst was successfully synthesized by a facile method. The samples were characterized by X-ray photoelectron spectrometry (XPS), X-ray diffractometry (XRD), field-emission scanning electron microscopy (FE-SEM), UV-Vis diffuse spectroscopy (DRS), Fourier transform infrared spectroscopy (FTIR), and N adsorption-desorption isotherms. In order to check the catalytic efficiencies toward reduction reaction, 4-nitrophenol (4-NP) and other organic dyes such as rhodamine-B (RhB), methylene blue (MB), and methyl orange (MO) were used.

Cancer stem-like cells directly participate in vasculogenic mimicry channels in triple-negative breast cancer.

Objective: Vasculogenic mimicry (VM) channels that are lined by tumor cells are a functional blood supply in malignant tumors. However, the role of VM-initiating cells remains poorly understood. Cancer stem-like cells (CSCs) are positively correlated with VM.

NDRG1 suppresses vasculogenic mimicry and tumor aggressiveness in gastric carcinoma.

N-myc downstream regulated gene 1 (NDRG1) has been well characterized as a suppressor of metastasis in numerous types of carcinoma. NDRG1 inhibits the metastatic progression of cancer cells via its inhibitory effects on a wide variety of cellular signaling pathways. Vasculogenic mimicry (VM) refers to the unique ability of aggressive tumor cells to mimic the pattern of embryonic vasculogenic networks, and is the main reason for the poor prognosis and failure of antivascular therapy in gastric carcinoma (GC).

S1PR1 regulates the switch of two angiogenic modes by VE-cadherin phosphorylation in breast cancer.

Angiogenesis in solid tumors is divided into two modes: endothelium-dependent vessel (EDV) and vasculogenic mimicry (VM). Sphingosine-1-phosphate receptor 1 (S1PR1) plays a vital role on EDV in a variety of human tumors. However, the relationship between S1PR1 and VM is not clear.

Concurrent Optical Gain Optimization and Electrical Tuning in Novel Oligomer:Polymer Blends with Yellow-Green Laser Emission.

Electrically pumped organic lasing requires the integration of electrodes contact into the laser cavity in an organic light-emitting diode (OLED) or organic field effect transistor configuration to enable charge injection. Efficient and balanced carrier injection requires in turn alignment of the energy levels of the organic active layers with the Fermi levels of the cathode and anode. This can be achieved through chemical substitution with specific aromatic functional groups, although paying the price for a substantial (and often detrimental) change in the emission and light amplifying properties of the organic gain medium.

The suppression of DUSP5 expression correlates with paclitaxel resistance and poor prognosis in basal-like breast cancer.

Basal-like breast cancer (BLBC) is resistant to endocrinotherapy and targeted therapy and new molecular therapies are needed for BLBC. In this study, we evaluated the role of DUSP1 and DUSP5, negative regulators of mitogen-activated protein kinase pathway, in the aggressiveness of BLBC. MDA-MB-231 cells were given paclitaxel (PTX) treatment and subsequently PTX resistant cell clones were established.

TP53INP1 inhibits hypoxia-induced vasculogenic mimicry formation via the ROS/snail signalling axis in breast cancer.

Tumour protein p53-inducible nuclear protein 1 (TP53INP1) is a tumour suppressor associated with malignant tumour metastasis. Vasculogenic mimicry (VM) is a new tumour vascular supply pattern that significantly influences tumour metastasis and contributes to a poor prognosis. However, the molecular mechanism of the relationship between TP53INP1 and breast cancer VM formation is unknown.

Effect of follicle cell autophagy on gonadal development of triploid female rainbow trout (Oncorhynchus mykiss).

Autophagy is a cellular process which occurs in eukaryotic cells. To study the mechanism regulating polyploid fish growth and development is of significance in genetic, because of its growth advantages and economic values. This study focused on triploid female rainbow trout (RBT) which discusses the effects of autophagy on gonadal development of polyploid fish.

TRA2A Promoted Paclitaxel Resistance and Tumor Progression in Triple-Negative Breast Cancers via Regulating Alternative Splicing.

Treatment of triple-negative breast cancer (TNBC) has been challenging, and paclitaxel resistance is one of the major obstacles to the better prognosis. Deregulation of alternative splicing (AS) may contribute to tumor progression and chemotherapy resistance. Human AS factor has two separate gene paralogs encoding TRA2A and TRA2B proteins.