Integration of single-cell transcriptomics and bulk transcriptomics to explore prognostic and immunotherapeutic characteristics of nucleotide metabolism in lung adenocarcinoma.

Background: Lung adenocarcinoma (LUAD) is a highly aggressive tumor with one of the highest morbidity and mortality rates in the world. Nucleotide metabolic processes are critical for cancer development, progression, and alteration of the tumor microenvironment. However, the effect of nucleotide metabolism on LUAD remains to be thoroughly investigated.

PGD2/PTGDR2 signaling pathway affects the self-renewal capacity of gastric cancer stem cells by regulating ATG4B ubiquitination.

Background: Prostaglandin D2 (PGD2) inhibits the development of different malignant tumors; however, the underlying mechanism of inhibiting tumor development is not yet clear. This study aimed to elucidate how PGD2 inhibits the stemness of gastric cancer stem cells (GCSCs) autophagy and its underlying molecular mechanism to provide a theoretical basis for the treatment of gastric cancer.

Methods: In this study, GCSCs were enriched by serum-free incubation.

Development of a novel centrosome-related risk signature to predict prognosis and treatment response in lung adenocarcinoma.

Background: Abnormalities of centrosomes, the major microtubular organizing centers of animal cells and regulators of cell cycle progression, usually accelerate tumor progression, but their prognostic value in lung adenocarcinoma (LUAD) remains insufficiently explored.

Methods: We collected centrosome genes from the literature and identified LUAD-specific centrosome-related genes (CRGs) using the single-sample gene set enrichment analysis (ssGSEA) algorithm and weighted gene co-expression network analysis (WGCNA). Univariate Cox was performed to screen prognostic CRGs.

Integration of the bulk transcriptome and single-cell transcriptome reveals efferocytosis features in lung adenocarcinoma prognosis and immunotherapy by combining deep learning.

Background: Efferocytosis (ER) refers to the process of phagocytic clearance of programmed dead cells, and studies have shown that it is closely related to tumor immune escape.

Methods: This study was based on a comprehensive analysis of TCGA, GEO and CTRP databases. ER-related genes were collected from previous literature, univariate Cox regression was performed and consistent clustering was performed to categorize lung adenocarcinoma (LUAD) patients into two subgroups.

Identification of a novel immunogenic death-associated model for predicting the immune microenvironment in lung adenocarcinoma from single-cell and Bulk transcriptomes.

Studies on immunogenic death (ICD) in lung adenocarcinoma are limited, and this study aimed to determine the function of ICD in LUAD and to construct a novel ICD-based prognostic model to improve immune efficacy in lung adenocarcinoma patients. The data for lung adenocarcinoma were obtained from the Cancer Genome Atlas (TCGA) database and the National Center for Biotechnology Information (GEO). The single-cell data were obtained from Bischoff P et al.

Investigating the mechanism and the effect of aquaporin 5 (AQP5) on the self-renewal capacity of gastric cancer stem cells.

Aquaporin 5 (AQP5) has been shown to have a pro-carcinogenic effect in numerous types of malignancies. This research intends to investigate the role and the molecular mechanism of AQP5 on enriched gastric cancer stem cells (GCSCs). : Immunohistochemistry, western blot (WB), and RT-qPCR techniques were employed to identify the presence of AQP5 in gastric cancer (GC) and the neighboring paracancerous tissues.

Elucidating the mechanism of action of Isobavachalcone induced autophagy and apoptosis in non-small cell lung cancer by network pharmacology and experimental validation methods.

Background: Lung cancer is the leading cause of cancer deaths, and non-small cell lung cancer (NSCLC) accounts for the majority of lung cancer-related mortality. In recent years, there have been numerous treatments for non-small cell lung cancer, but the cure and survival rates are still extremely low. Isobavachalcone (IBC) belongs to the chalcone component of the traditional Chinese medicine Psoralea corylifolia L.

The critical role of residues Phe120 and Val161 of (2 R,3 R)‑2,3‑butanediol dehydrogenase from Neisseria gonorrhoeae as probed by molecular docking and site-directed mutagenesis.

NAD-dependent (2 R,3 R)‑2,3‑butanediol dehydrogenase (BDH) from Neisseria gonorrhoeae (NgBDH) is a representative member of the medium-chain dehydrogenase/reductase (MDR) superfamily. To date, little information is available on the substrate binding sites and catalytic residues of BDHs from this superfamily. In this work, according to molecular docking studies, we found that conserved residues Phe120 and Val161 form strong hydrophobic interactions with both (2 R,3 R)‑2,3‑butanediol (RR-BD) and meso-2,3‑butanediol (meso-BD) and that mutations of these residues to alanine or threonine impair substrate binding.

Copper-binding protein modelling by single-cell transcriptome and Bulk transcriptome to predict overall survival in lung adenocarcinoma patients.

Copper and copper-binding proteins are key components of tumour progression as they play an important role in tumour invasion and migration, and abnormal accumulation of copper (Cu) may be intimately linked to with lung adenocarcinoma (LUAD). Data on lung adenocarcinoma were sourced from the Cancer Genome Atlas (TCGA) database and the National Centre for Biotechnology Information (GEO). 10x scRNA sequencing, which is from Bischoff P et al, was used for down-sequencing clustering and subgroup identification using TSNE.

Identification of T-cell exhaustion-related genes and prediction of their immunotherapeutic role in lung adenocarcinoma.

Lung adenocarcinoma ranks as the second most widespread form of cancer globally, accompanied by a significant mortality rate. Several studies have shown that T cell exhaustion is associated with immunotherapy of tumours. Consequently, it is essential to comprehend the possible impact of T cell exhaustion on the tumor microenvironment.

Multi-omics identification of GPCR gene features in lung adenocarcinoma based on multiple machine learning combinations.

Lung adenocarcinoma is a common malignant tumor that ranks second in the world and has a high mortality rate. G protein-coupled receptors (GPCRs) have been reported to play an important role in cancer; however, G protein-coupled receptor-associated features have not been adequately investigated. In this study, GPCR-related genes were screened at single-cell and bulk transcriptome levels based on AUcell, single-sample gene set enrichment analysis (ssGSEA) and weighted gene co-expression network (WGCNA) analysis.

PBK correlates with prognosis, immune escape and drug response in LUAD.

PBK (PDZ-binding kinase) is a protein-coding gene that encodes a serine/threonine protein kinase associated with the dual-specific mitogen-activated protein kinase (MAPKK) family. Overexpression of this gene is closely linked to tumor development. In this study, we aimed to investigate the role of PBK in lung adenocarcinoma (LUAD) progression, prognosis, and immune evasion.

Predicting lung adenocarcinoma prognosis, immune escape, and pharmacomic profile from arginine and proline-related genes.

Lung adenocarcinoma (LUAD) is a highly heterogeneous disease that ranks first in morbidity and mortality. Abnormal arginine metabolism is associated with inflammatory lung disease and may influence alterations in the tumor immune microenvironment. However, the potential role of arginine and proline metabolic patterns and immune molecular markers in LUAD is unclear.

Nosip is a potential therapeutic target in hepatocellular carcinoma cells.

Nitric oxide synthase-interacting protein (Nosip) interacts with nitric oxide synthase (NOS) and regulates NO synthesis and release, which participates in various critical physiological and pathological processes. However, the role of Nosip in hepatocellular carcinoma (HCC) is unclear. In this study, Nosip expression was found to be elevated in HCC tissues and cells.

Nitidine Chloride Triggers Autophagy and Apoptosis of Ovarian Cancer Cells through Akt/mTOR Signaling Pathway.

Objective: Ovarian cancer (OC) is the eighth most common cancer with high mortality in women worldwide. Currently, compounds derived from Chinese herbal medicine have provided a new angle for OC treatment.

Methods: In this study, the cell proliferation and migration of ovarian cancer A2780/SKOV3 cells were inhibited after being treated with nitidine chloride (NC) by using MTT and Wound-Healing Assay.

Regulation of early diagnosis and prognostic markers of lung adenocarcinoma in immunity and hypoxia.

Lung adenocarcinoma is still cancer with the highest mortality. Hypoxia and immunity play an essential role in the occurrence and development of tumors. Therefore, this study is mainly to find new early diagnosis and prognosis markers and explore the relationship among the markers and immunity and hypoxia, to improve the prognosis of patients.

B cell-related tertiary lymphoid structure may exert inhibitory effects on lung adenocarcinoma and SARS-COV-2.

Background: The prognosis of lung adenocarcinoma (LUAD) is poor. Infection with coronavirus disease 2019 (COVID-19) may further worsen the outcome of LUAD. This study utilized the immune model and the COVID-19 receptor signal to identify the potential immune structure affecting the prognosis of COVID-19 and LUAD.

PDS5B inhibits cell proliferation, migration, and invasion via upregulation of LATS1 in lung cancer cells.

PDS5B (precocious dissociation of sisters 5B) plays a pivotal role in carcinogenesis and progression. However, the biological functions of PDS5B in lung cancer and its underlying mechanisms are not fully elucidated. In the present study, we used MTT assays, wound-healing assays, and transwell migration and invasion approach to examine the cell viability, migration, and invasion of non-small cell lung cancer (NSCLC) cells after PDS5B modulation.

Orlistat induces ferroptosis-like cell death of lung cancer cells.

Aberrant de novo lipid synthesis is involved in the progression and treatment resistance of many types of cancers, including lung cancer; however, targeting the lipogenetic pathways for cancer therapy remains an unmet clinical need. In this study, we tested the anticancer activity of orlistat, an FDA-approved anti-obesity drug, in human and mouse cancer cells in vitro and in vivo, and we found that orlistat, as a single agent, inhibited the proliferation and viabilities of lung cancer cells and induced ferroptosis-like cell death in vitro. Mechanistically, we found that orlistat reduced the expression of GPX4, a central ferroptosis regulator, and induced lipid peroxidation.