Retinol Saturase Mediates Retinoid Metabolism to Impair a Ferroptosis Defense System in Cancer Cells.

Unlabelled: Ferroptosis is an iron-dependent form of regulated cell death induced by the lethal overload of lipid peroxides in cellular membranes. In recent years, modulating ferroptosis has gained attention as a potential therapeutic approach for tumor suppression. In the current study, retinol saturase (RETSAT) was identified as a significant ferroptosis mediator using a publicly accessible CRISPR/Cas9 screening dataset.

Hepatic nuclear factor 4 alpha promotes the ferroptosis of lung adenocarcinoma transcriptional activation of cytochrome P450 oxidoreductase.

Background: Lung adenocarcinoma is one of the most prevalent cancers while ferroptosis is crucial for cancer therapies. This study aims to investigate the function and mechanism of hepatic nuclear factor 4 alpha (HNF4A) in lung adenocarcinomas' ferroptosis.

Materials And Methods: HNF4A expression in ferroptotic A549 cells was detected.

The immunomodulatory role of all-trans retinoic acid in tumor microenvironment.

Retinoids are essential nutrients for human beings. Among them, all-trans retinoic acid (ATRA), considered one of the most active metabolites, plays important roles in multiple biological processes. ATRA regulates the transcription of target genes by interacting with nuclear receptors bonded to retinoic acid response elements (RAREs).

miR-6077 promotes cisplatin/pemetrexed resistance in lung adenocarcinoma via CDKN1A/cell cycle arrest and KEAP1/ferroptosis pathways.

Lung adenocarcinoma (LUAD) is one of the most common malignancies worldwide. Combination chemotherapy with cisplatin (CDDP) plus pemetrexed (PEM) remains the predominant therapeutic regimen; however, chemoresistance greatly limits its curative potential. Here, through CRISPR-Cas9 screening, we identified miR-6077 as a key driver of CDDP/PEM resistance in LUAD.

Genomic And Tumor Microenvironment Differences Between Cell Cycle Progression Pathway Altered/Non-Altered Patients With Lung Adenocarcinoma.

Background: Identified as a hallmark of cancer, the dysregulated cell cycle progression plays an important role in the promotion and progression of lung adenocarcinoma (LUAD). However, the genomic and microenvironment differences between cell cycle progression pathway altered/non-altered LUAD patients remain to be elucidated.

Materials And Methods: Data of this study were obtained from The Cancer Genome Atlas (TCGA), including simple nucleotide variation, copy number variation (CNV), RNA-seq gene expression, miRNA expression, survival, and clinical information.

Multi-Omics Analysis of Cancer Cell Lines with High/Low Ferroptosis Scores and Development of a Ferroptosis-Related Model for Multiple Cancer Types.

Ferroptosis is a newly identified regulated cell death characterized by iron-dependent lipid peroxidation and subsequent membrane oxidative damage, which has been implicated in multiple types of cancers. The multi-omics differences between cancer cell lines with high/low ferroptosis scores remain to be elucidated. We used RNA-seq gene expression, gene mutation, miRNA expression, metabolites, copy number variation, and drug sensitivity data of cancer cell lines from DEPMAP to detect multi-omics differences associated with ferroptosis.

Differences in genetics and microenvironment of lung adenocarcinoma patients with or without TP53 mutation.

Background: Differences in genetics and microenvironment of LUAD patients with or without TP53 mutation were analyzed to illustrate the role of TP53 mutation within the carcinogenesis of LUAD, which will provide new concepts for the treatment of LUAD.

Methods: In this study, we used genetics and clinical info from the TCGA database, including somatic mutations data, RNA-seq, miRNA-seq, and clinical data. More than one bioinformatics tools were used to analyze the unique genomic pattern of TP53-related LUAD.

Clinicopathological and prognostic implications of ALK rearrangement in patients with completely surgically resected lung adenocarcinoma.

Background: The prognostic significance of ALK rearrangement is still contradictory. Here, we aimed to investigate the clinical characteristics and outcomes of lung adenocarcinoma patients with ALK rearrangement, and analyze whether these patients benefited from targeted therapy.

Methods: This was a retrospective cohort study of 80 ALK-rearranged lung adenocarcinoma patients who had undergone radical surgery and another 3031 ALK mutation-negative patients were retrospectively reviewed for inclusion in this case-controlled analyses.