Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Huaier Enhances the Antitumor Activities of Black Phosphorus and Alleviates Nephrotoxicity by Regulating Mitophagy and Autophagy

ABSTRACT: Huaier Enhances the Antitumor Activities of Black Phosphorus and Alleviates Nephrotoxicity by Regulating Mitophagy and Autophagy

PROVIDER: PRJNA952891 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR24091344_1.fastq.gz	Fastqsanger.gz
	SRR24091344_2.fastq.gz	Fastqsanger.gz
	SRR24091345_1.fastq.gz	Fastqsanger.gz
	SRR24091345_2.fastq.gz	Fastqsanger.gz
	SRR24091346_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Huaier Enhances the Antitumor Activities of Black Phosphorus and Alleviates Nephrotoxicity by Regulating Mitophagy and Autophagy

Project description:Black phosphorus (BP) has shown promise as a nanomaterial for cancer therapy, but its nephrotoxicity limits its use. To improve BP anti-tumor effects and reduced toxic side effects, this study presents a novel approach to cancer therapy by combining BP with the traditional Chinese medicine Trametes robiniophila Murr (Huaier) to improve the treatment outcome for pancreatic cancer, a highly fatal malignancy. In 2D/3D cell lines, patient-derived organoids (PDOs) and mouse model, Huaier extraction is demonstrated to the antitumor effects of BP and mitigates BP-induced nephrotoxicity. RNA-sequencing analysis revealed that the combination of BP and Huaier enriched the mitophagy and ferroptosis pathways. While BP activates the mitophagy pathway to recycle damaged mitochondria, Huaier accelerates BP-induced mitochondrial dysfunction, leading to a mitochondrial burst and ultimately activating ferroptosis in PAAD cells. Furthermore, Huaier mitigates BP-induced nephrotoxicity and recovers cell viability by modulating the level of autophagy in proximal tubule epithelial cells. By synergizing BP with Huaier, we have achieved more potent antitumor activities with lower nephrotoxicity. These findings provide a promising strategy for treating PAAD in in vitro and in vivo models.

2023-08-01 | GSE229091 | GEO

Activating Parkin-dependent mitophagy alleviates oxidative stress, apoptosis, and promotes random-pattern skin flaps survival

Project description:The random-pattern skin flap is a crucial technique in reconstructive surgery and flap necrosis caused by ischemia/reperfusion injury is a major postoperative complication. Herein, we investigated the mechanism of mitophagy induced by Melatonin (ML) and its effect on the survival of skin flaps. Our results demonstrated that ML could activate mitophagy, ameliorate oxidative stress and alleviate apoptosis in TBHP-stimulated human umbilical vein endothelial cells in vitro. Inhibiting ML-induced mitophagy considerably abolished its protective effects. Moreover, knockdown of Parkin by siRNA inhibited ML-induced mitophagy, and subsequently exacerbated oxidative stress and apoptosis. Further study demonstrated that inhibition of AMPK reversed these protective effects of ML and downregulated the expression of TFEB. In the vivo study, ML effectively promoted flap survival by activating mitophagy and subsequently ameliorating oxidative stress and mitigating apoptosis. These results established that ML is a potent agent capable for increasing random-pattern skin flap survival by activating Parkin-dependent mitophagy through the AMPK-TFEB signaling pathway.

2022-06-29 | GSE203609 | GEO

Single-nucleus transcriptional profiling of chronic kidney disease after cisplatin nephrotoxicity

Project description:Cisplatin induces both acute and chronic nephrotoxicity during chemotherapy in cancer patients. Here, we report the study of single-nucleus sequencing (snRNA-seq) of cisplatin-induced nephrotoxicity.

2023-08-05 | GSE239749 | GEO

Cold-catalytic antitumor immunity with pyroelectric black phosphorus nanosheets.

Project description:Catalytic nanomedicine with the innate features of catalysts brings incomparable properties to biomedicine over traditional drugs. The temperature-dependent activity of catalysts provides catalytic nanomedicines with a facile strategy to control their therapeutic performance. Tuning catalytic nanomedicine by cold treatment (4-37 °C) is safe and desired for practical applications, but there is a lack of cold-catalytic platforms. Herein, with black phosphorus (BP) as a model pyroelectric nanocatalyst, we explored the potential of cold-catalysts for antitumor therapy. BP nanosheets with pyro-catalytic activity catalyze the generation of oxidative stress to activate antitumor immunity under cold treatment. Due to the cold-catalytic immunomodulation, immune memory was successfully achieved to prevent tumor metastasis and recurrence. Considering the safety and conductive depth (>10 mm) of cold in the body, pyroelectric nanocatalysts open up exciting opportunities for the development of cold-catalytic nanomedicine.

| S-EPMC9200116 | biostudies-literature

Polymyxin nephrotoxicity in kidney chip

Project description:Polymyxin nephrotoxicity in kidney chip

| PRJNA508797 | ENA

Biomarkers for aristolochic acid nephrotoxicity

Project description:Biomarkers for aristolochic acid nephrotoxicity

| PRJNA680917 | ENA

MicroRNA profiling of rats with ochratoxin A nephrotoxicity

Project description:The objective of this study is to analyze miRNA profiling in the kidneys of rats gavaged with OTA. To profile miRNAs in the kidneys of rats with OTA nephrotoxicity, high-throughput sequencing and bioinformatics approaches were applied to analyze the miRNAs in the kidney of rats following OTA treatment

2014-06-01 | E-MTAB-2475 | biostudies-arrayexpress

Boosting Antitumor Sonodynamic Therapy Efficacy of Black Phosphorus via Covalent Functionalization.

Project description:Sonodynamic therapy (SDT) triggered by ultrasound represents an emerging tumor therapy approach with minimally invasive treatment featuring nontoxicity and deep tissue-penetration, and its efficacy sensitively depends on the sonosensitizer which determines the generation of reactive oxygen species (ROS). Herein, for the first time covalently functionalized few-layer black phosphorus nanosheets (BPNSs) are applied as novel sonosensitizers in SDT, achieving not only boosted SDT efficacy but also inhibited cytotoxicity relative to the pristine BPNSs. Three different covalently functionalized-BPNSs are synthesized, including the first fullerene-functionalized BPNSs with C60 covalently bonded onto the surface of BPNSs (abbreviated as C60 -s-BP), surface-functionalized BPNSs by benzoic acid (abbreviated as BA-s-BP), and edge-functionalized BPNSs by C60 (abbreviated as C60 -e-BP), and the role of covalent functionalization pattern of BPNSs on its SDT efficacy is systematically investigated. Except C60 -e-BP, both surface-functionalized BPNSs (C60 -s-BP, BA-s-BP) exhibit higher SDT efficacies than the pristine BPNSs, while the highest SDT efficacy is achieved for BA-s-BP due to its strongest capability of generating the hydroxyl (·OH) radicals, which act as the dominant ROS to kill the tumor cells.

| S-EPMC8529424 | biostudies-literature

Nitazoxanide impairs mitophagy flux through ROS-mediated mitophagy initiation and lysosomal dysfunction in bladder cancer

Project description:Bladder cancer is one of the most common malignancy in the urinary tract with high recurrence and drug resistance in clinics. Alternative treatments from existing drugs might be a promising strategy. Nitazoxanide (NTZ), an FDA-approved antiprotozoal drug, has got increasingly noticed because of its favorable safety profile and antitumor potential, yet the effects in bladder cancer and underlying mechanisms remain poorly understood. Herein, we find that NTZ induces mitochondrial damage and mitophagy initiation through PINK1-generated phospho-ubiquitin(pS65-Ub) and autophagy receptor-mediated pathway even in the absence of Atg5/Beclin1. Meanwhile, NTZ inhibits lysosomal degradation activity, leading to mitophagy flux impairment at late stage. Mitochondrial reactive oxygen species (ROS) production is critical in this process, as eliminating ROS with N-acetylcysteine (NAC) efficiently inhibits PINK1 signaling-mediated mitophagy initiation and alleviates lysosomal dysfunction. Co-treatment with NTZ and autophagy inhibitor Chloroquine (CQ) to aggravate mitophagy flux impairment promotes NTZ-induced apoptosis, while alleviation of mitophagy flux impairment with ROS scavenger reduced cell death. Moreover, we also discover a similar signaling response in the 3D bladder tumor spheroid after NTZ exposure. In vivo study reveals a significant inhibition of orthotopic bladder tumors with no obvious systemic toxicity. Together, our results uncover the anti-tumor activities of NTZ with the involvement of ROS-mediated mitophagy modulation at different stages and demonstrate it as a potential drug candidate for fighting against bladder tumors.

2021-03-31 | GSE171129 | GEO

Pairwise multiplex CRISPR/Cas9 screen of mitophagy receptors in acute myeloid leukemia

Project description:The selective autophagic degradation of mitochondria via mitophagy is essential for preserving mitochondrial homeostasis and thereby disease maintenance and progression in acute myeloid leukemia. The process of mitophagy is orchestrated by a variety of mitophagy receptors whose interplay in AML is not well understood. Here, we established a dual multiplexed CRISPR screen targeting mitophagy receptors to elucidate redundancies and individual contributions of mitophagy receptors and gain a deeper understanding of the functional interactome governing mitophagy in AML.

2023-07-11 | GSE211073 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data