Biomimetic nanocrystals co-deliver paclitaxel and small-molecule LF3 for ferroptosis-combined chemotherapy for gastric cancer.

Combination chemotherapy is considered more effective than monotherapy in enhancing clinical outcomes. Ferroptosis, a unique form of regulated cell death, has been demonstrated to inhibit tumor growth and progression. Consequently, combining ferroptosis with chemotherapy represents a promising and innovative approach to antitumor therapy.

Identification of GRIN2D as a novel therapeutic target in pancreatic ductal adenocarcinoma.

Background: Pancreatic ductal adenocarcinoma (PDAC) is a devastating disease with a dismal prognosis, and despite significant advances in our understanding of its genetic drivers, like KRAS, TP53, CDKN2A, and SMAD4, effective therapies remain limited. Here, we identified a new therapeutic target GRIN2D and then explored its functions and mechanisms in PDAC progression.

Methods: We performed a genome-wide RNAi screen in a PDAC xenograft model and identified GRIN2D, which encodes the GluN2D subunit of N-methyl-D-aspartate receptors (NMDARs), as a potential oncogene.

Improved strategy for post-traumatic hydrocephalus following decompressive craniectomy: Experience of a single center.

Background: Patients with head trauma may develop hydrocephalus after decompressive craniectomy. Many studies have referred one-stage cranioplasty (CP) and ventriculoperitoneal shunt (VPS) was applied to treat cranial defect with post-traumatic hydrocephalus (PTH), but the safety and efficiency of the procedure remain controversial.

Methods: This is a retrospective cohort study including 70 patients of PTH following decompressive craniectomy who underwent simultaneous (50) and separated (20) procedures of cranioplasty and VPS from March 2014 to March 2021 at the authors' institution with at least 30 days of follow-up.

A tumor-suppressive circular RNA mediates uncanonical integrin degradation by the proteasome in liver cancer.

Circular RNAs (circRNAs) have emerged as important regulators of various cellular processes and have been implicated in cancer. Previously, we reported the discovery of several dysregulated circRNAs including circPABPC1 (polyadenylate-binding protein 1) in human hepatocellular carcinoma (HCC), although their roles in HCC development remained unclear. Here, we show that circPABPC1 is preferentially lost in tumor cells from clinical samples and inhibits both intrahepatic and distant metastases in a mouse xenograft model.

The Beneficial Effects of Quercetin, Curcumin, and Resveratrol in Obesity.

Over the past two decades, obesity has been one of the major public health concerns in most countries. In the search for new molecules that could be used for the treatment of obesity, good perspectives have been opened up for polyphenols, a class of natural bioactive phytochemicals. Experimental and limited clinical trial evidence supports that some polyphenols such as quercetin, curcumin, and resveratrol have potential benefit functions on obesity treatment.

Comprehensive molecular profiling of the B7 family of immune-regulatory ligands in breast cancer.

The B7 gene family has crucial roles in the regulation of adaptive cellular immunity. In cancer, deregulation of co-inhibitory B7 molecules is associated with reduced antitumor immunity and cancer immune evasion. FDA approval of cancer immunotherapy antibodies against cytotoxic T lymphocyte-associated protein 4 (CTLA-4) and programmed cell death-1 (PD-1)-both ligands of the B7 family-demonstrate the impact of these checkpoint regulators in cancer.

LRIG1 dictates the chemo-sensitivity of temozolomide (TMZ) in U251 glioblastoma cells via down-regulation of EGFR/topoisomerase-2/Bcl-2.

In the current study, we aimed to understand the potential role of leucine-rich repeats and immunoglobulin-like domains 1 (LRIG1) in TMZ-resistance of U251 glioma cells. We established TMZ-resistant U251 clones (U251/TMZ cells), which expressed low level of LRIG1, but high levels of epidermal growth factor receptor (EGFR), topoisomerase-2 (Topo-2) and Bcl-2. Depletion of LRIG1 by the targeted RNA interference (RNAi) upregulated EGFR/Topo-2/Bcl-2 in U251 cells, and the cells were resistant to TMZ.

Enhancer of zeste homolog 2 silences microRNA-218 in human pancreatic ductal adenocarcinoma cells by inducing formation of heterochromatin.

Background & Aims: Enhancer of zeste homolog 2 (EZH2) is a histone methyltransferase that is overexpressed by pancreatic ductal adenocarcinoma (PDAC) cells and increases their aggressiveness. We identified microRNAs (miRs) that are regulated by EZH2 and studied their functions in PDAC cells.

Methods: We performed miR profile analysis of PDAC cells incubated with EZH2 inhibitor 3-deazaneplanocin A, and pancreatic ductal epithelial cells that overexpressed EZH2.

A predicted miR-27a-mediated network identifies a signature of glioma.

The dysregulation of physiological microRNA (miRNA) activity has been shown to play an important role in gliomagenesis. In a previous study, using microRNA arrays and glioma tissues found that miR-27a was upregulated, which was also identified in the glioma cell lines and samples by quantitative real-time polymerase chain reaction (qRT-PCR). In this study, in order to explore the potential roles of miR-27a in the progression of glioma, we first utilized text-mining of PubMed abstracts with natural language processing (NLP) to identify 1,168 glioma-related molecules.

miR-92a is a critical regulator of the apoptosis pathway in glioblastoma with inverse expression of BCL2L11.

Recent studies have revealed that miR-92a is overexpressed in several types of malignancies and provides a protumorigenic effect. Our findings demonstrate that the high expression of miR-92a in human glioma specimens is significantly correlated with low levels of BCL2L11 (Bim) protein and high-grade glioma. Here, we present the first evidence that miR-92a antisense oligonucleotide (AS-miR-92a) provides a tumor suppressive effect via induction of apoptosis in human glioma cells.

Correlation of epigenetic aberrance with STAT3 signaling pathway in gastric carcinogenesis.

Background: It has been suggested that STAT3 signaling plays important roles in regulating epigenetic aberrance during tumorigenesis, especially in the expression of certain key epigenetic enzymes such as DNMTs, HDACs, and HMTs. However, there has been no report on the relationship of STAT3 signaling and epigenetic aberrance in gastrocarcinogenesis.

Aim: The purpose of this study was to explore the interrelationship of STAT3 signaling pathway and epigenetic aberrance in gastrocarcinogenesis.