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Isovalerylspiramycin I suppresses small cell lung cancer growth via ROS-mediated DNA damage and ER Stress

ABSTRACT: Isovalerylspiramycin I suppresses small cell lung cancer growth via ROS-mediated DNA damage and ER Stress

PROVIDER: PRJNA1022487 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26225340_1.fastq.gz	Fastqsanger.gz
	SRR26225340_2.fastq.gz	Fastqsanger.gz
	SRR26225341_1.fastq.gz	Fastqsanger.gz
	SRR26225341_2.fastq.gz	Fastqsanger.gz
	SRR26225342_1.fastq.gz	Fastqsanger.gz

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Isovalerylspiramycin I suppresses small cell lung cancer growth via ROS-mediated DNA damage and ER Stress

Project description:Characterized by rapid progression, early metastasis, and poor prognosis, small cell lung cancer (SCLC) is a highly malignant tumor with limited treatment breakthroughs for nearly 30 years. Exploring alternative approaches is urgent. Tumor cells are more susceptible to ROS triggers for they have a fragile redox balance compared to normal cells. Isovalerylspiramycin I (ISP-I)， purified from a novel macrolide antibiotic carrimycin， inducing accumulation of ROS in several tumor cells, has shown impressive anti-tumor potential. While the specific details and mechanisms of ISP-I's anti-SCLC effects remain unrevealed. We demonstrated that, ISP-I inhibited SCLC growth dose-dependently in vitro and in vivo, with good safety profiles for showing low toxicity to normal cells (MRC-5) and mice at therapeutic doses. Then, we utilized SCLC cell lines H1048 and DMS53 to uncover the anti-SCLC mechanisms of ISP-I. Primarily, ISP-I acted as an inducer of ROS, leading to H1048 and DMS53 cells DNA damage and endoplasmic reticulum (ER) stress through ROS accumulation， ultimately resulting in tumor cells G2/M cell cycle arrest and apoptosis. In conclusion, our study has proven that ISP-I may be a promising therapeutic approach for SCLC with good safety profiles.

2023-10-10 | GSE244376 | GEO

Pexophagy suppresses ROS-induced damage in leaf cells under high-intensity light

Project description:Although light is essential for photosynthesis, it has the potential to elevate intracellular levels of reactive oxygen species (ROS). Since high ROS levels are cytotoxic, plants must alleviate such damage. However, the cellular mechanism underlying ROS-induced leaf damage alleviation in peroxisomes was not fully explored. Here, we show that autophagy plays a pivotal role in the selective removal of ROS-generating peroxisomes, which protects plants from oxidative damage during photosynthesis. We present that autophagy-deficient mutants show light intensity-dependent leaf damage and excess aggregation of ROS-accumulating peroxisomes. The peroxisome aggregates are specifically engulfed by pre-autophagosomal structures and vacuolar membranes in both leaf cells and isolated vacuoles, but they are not degraded in mutants. ATG18a-GFP and GFP-2×FYVE, which bind to phosphatidylinositol 3-phosphate, preferentially target the peroxisomal membranes and pre-autophagosomal structures near peroxisomes in ROS-accumulating cells under high-intensity light. Our findings provide deeper insights into the plant stress response caused by light irradiation.

2023-02-27 | PXD038480 | Pride

Post-translational Modification of RNA m6A Demethylase ALKBH5 Regulates ROS-induced DNA Damage Response

Project description:Faithful genome integrity maintenance plays an essential role in cell survival. Here, we identify the RNA demethylase ALKBH5 as a key regulator that protects cells from DNA damage and apoptosis during reactive oxygen species (ROS)-induced stress. We find that ROS significantly induces global mRNA N6-methyladenosine (m6A) levels by modulating ALKBH5 post-translational modifications (PTMs), leading to the rapid and efficient induction of thousands of genes involved in a variety of biological processes including DNA damage repair. Mechanistically, ROS promotes ALKBH5 SUMOylation through activating ERK/JNK signaling, leading to inhibition of ALKBH5 m6A demethylase activity by blocking substrate accessibility. Moreover, ERK/JNK/ALKBH5-PTMs/m6A axis is activated by ROS in hematopoietic stem/progenitor cells (HSPCs) in vivo in mice, suggesting a physiological role of this molecular pathway in the maintenance of genome stability in HSPCs. Together, our study uncovers a molecular mechanism involving ALKBH5 PTMs and increased mRNA m6A levels that protect genomic integrity of cells in response to ROS.

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ER-associated degradation ligase HRD1 links ER stress to DNA damage repair by modulating the activity of DNA-PKcs

Project description:ER-associated degradation ligase HRD1 links ER stress to DNA damage repair by modulating the activity of DNA-PKcs

2024-08-20 | PXD055020 |

ER stress impairs the insulin signaling pathway through mitochondrial damage in SH-SY5Y human neuroblastoma cells

Project description:This SuperSeries is composed of the following subset Series: GSE24497: ER stress impairs the insulin signaling pathway through mitochondrial damage in SH-SY5Y human neuroblastoma cells (part 1) GSE24499: ER stress impairs the insulin signaling pathway through mitochondrial damage in SH-SY5Y human neuroblastoma cells (part 2) Refer to individual Series

2010-10-07 | E-GEOD-24500 | biostudies-arrayexpress

ROS-Responsive Potassium Ionophore-Based Nanoplatform Potentiates Cancer Pyroptosis-Immunotherapy via ER Stress

Project description:Pyroptosis is an emerging programmed cell death with great potential in antitumor immunotherapy. However, the actual application of pyroptosis is hampered by its nonspecificity and inefficiency. In this study, a reactive oxygen species (ROS) responsive potassium (K+) ionophore-based nanoplatform rPPAA18C6 is constructed based on the triblock polymers PEG-PPBAEM-PAA18C6 to potentiate cancer pyroptosis and immunotherapy via the K+ metabolic disturbance mediated endoplasmic reticulum (ER) stress. The PEG (P) is used to prolong the circulation time in vivo, PPBAEM (r) is used to target the tumor cells and responds to the higher ROS, and PAA18C6 is used to perturb of K+ homeostasis. Moreover, rPPAA18C6 can also function as a drug carrier for chemodrug (doxorubicin, Dox). We find that rPPAA18C6@Dox provokes immune responses in melanoma (B16F10) via pyroptosis-related immunogenic cell death (ICD), in which damage-associated molecular patterns (DAMPs) are released to promote maturation of dendritic cells (DCs), activate cytotoxic T lymphocytes (CTLs), and convert immunosuppressive “cold” tumor to immunogenic “hot” tumor. Moreover, the combined therapy with anti-PD-L1 exhibits apparent tumor suppression far more than expected, suggesting a powerful candidate of rPPAA18C6@Dox for high-efficient immune checkpoint blockade (ICB) therapy. This study thus provides a promising strategy to specifically initiate pyroptosis and potentiate immunotherapy by perturbation of K+ metabolism via a smart nanoplatform.

2025-01-01 | GSE256169 | GEO

Epigenetic therapy suppresses tumour growth by rewiring ER-mediated long-range chromatin interactions in ER+ endocrine-resistant breast cancer [HiC]

Project description:Epigenetic therapy suppresses tumour growth by rewiring ER-mediated long-range chromatin interactions in ER+ endocrine-resistant breast cancer [HiC]

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Epigenetic therapy suppresses tumour growth by rewiring ER-mediated long-range chromatin interactions in ER+ endocrine-resistant breast cancer [PCHiC]

Project description:Epigenetic therapy suppresses tumour growth by rewiring ER-mediated long-range chromatin interactions in ER+ endocrine-resistant breast cancer [PCHiC]

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Mitochondrial DNA quantity Counteracts ROS damage in oocytes during female reproductive aging

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ROS-Responsive Potassium Ionophore-Based Nanoplatform Potentiates Cancer Pyroptosis-Immunotherapy via ER Stress

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