Regulated Cell Death in Urinary Malignancies

Nie, Zhenyu; Chen, Mei; Gao, Yuanhui; Huang, Denggao; Cao, Hui; Peng, Yanling; Guo, Na; Zhang, Shufang

doi:10.3389/fcell.2021.789004

Cited by 15 publications

(13 citation statements)

References 186 publications

(264 reference statements)

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“…Separately, spatially localized expression of ERO1A , VDAC2 , ADM , and VEGFA were among the glycolysis and angiogenesis related genes identified when applying DREMI to the Glycolysis Activation in Cancer (Warburg Effect) gene module (Extended Data Fig. S6c) (59, 60). Both of these processes represent fundamental tumor promoting programs of hypoxic metabolism and promotion of tumor angiogenesis.…”

Section: Resultsmentioning

confidence: 99%

spARC recovers human glioma spatial signaling networks with graph filtering

Kuchroo

Miyagishima

Steach

et al. 2022

Preprint

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Biological networks operate within architectural frameworks that influence the state and function of cells through niche-specific factors such as exposure to nutrients and metabolites, soluble signaling molecules, and direct cognate cell-cell communication. Spatial omics technologies incorporate environmental information into the study of biological systems, where the spatial coordinates of cells may directly or indirectly encode these micro-anatomical features. However, they suffer from technical artifacts, such as dropout, that impede biological discovery. Current methods that attempt to correct for this fail to adequately integrate highly informative spatial information when recovering gene expression and modelling cell-cell dynamics \textit{in situ}. To address this oversight, we developed spatial Affinity-graph Recovery of Counts (spARC), a data diffusion-based filtration method that shares information between neighboring cells in tissue and related cells in expression space, to recover gene dynamics and simulate signalling interactions in spatial transcriptomics data. Following validation, we applied spARC to 10 IDH-mutant surgically resected human gliomas across WHO grades II-IV in order to study signaling networks across disease progression. This analysis revealed co-expressed genes that border the interface between tumor and tumor-infiltrated brain, allowing us to characterize global and local structure of glioma. By simulating paracrine signaling \textit{in silico}, we identified an Osteopontin-CD44 interaction enriched in grade IV relative to grade II and grade III astrocytomas, and validated the clinical relevance of this signaling axis using TCGA.

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Section: Resultsmentioning

confidence: 99%

spARC recovers human glioma spatial signaling networks with graph filtering

Kuchroo

Miyagishima

Steach

et al. 2022

Preprint

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“…Some RCD types have been found to correlate to multiple chemotherapeutic drugs in treating bladder cancer [78][79][80][81] . However, few mechanism studies were performed on RCD types in bladder cancer 82 . In our study, we preliminarily explored the cross-talk of ve types of RCD in bladder cancer by analyzing the mRNA expression correlation and protein-protein interaction.…”

Section: Discussionmentioning

confidence: 99%

The Cross-talk, Genetic Alteration, Molecular Functions, and Cluster Relevance of the Major Types of Regulated Cell Death in Bladder Cancer

Li¹,

Qi²,

Liu³

et al. 2022

Preprint

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The dysfunction of regulated cell death (RCD) could cause human diseases such as cancer, neurodegeneration, autoimmune diseases, and infectious diseases. Recent studies have indicated that RCD has closely functional interaction. Our study aimed to explore the cross-talk, genetic alteration, functions, mechanism, and cluster relevance of the several major types of RCD, including apoptosis, ferroptosis, pyroptosis, necroptosis, autophagy-dependent cell death, in bladder cancer (BLCA). Through analyzing the public database, we found that the genes representing these five RCD types showed complex cross-talk in mRNA, protein levels, somatic mutation, and DNA copy number in BLCA. The mRNA expression of regulated cell death genes (RCDGs) was affected by DNA copy number, somatic mutation, DNA methylation, and RNA modification. Several RCDGs were essential for cell viability, and the expression of RCDGs was correlated with radiotherapeutic sensitivity and IC50 of chemotherapy drugs. Based on the expression of RCDGs, the BLCA patients were divided into two clusters. We found multiple immune-related pathways significantly enriched in cluster1/cluster2. In addition, the patients' prognosis, immune therapy response, and drug sensitivity in these two clusters were significantly different. Through the comparison between the RCD clusters and consensus cluster, we found that RCD cluster1 mainly correlated with the basal squamous cluster, and the RCD cluster2 mainly correlated with the luminal cluster. Through the weighted gene co-expression network analysis (WGCNA), we identified the high correlation RCDGs with cluster1/cluster2. We found that most cluster1-RCDGs were correlated with poor prognosis for patients, and most prognosis-protection genes correlated with cluster2. Besides, the expression of these prognosis-related RCDGs showed different distribution patterns in basal/luminal subtypes. In summary, our study conducted a comprehensive analysis of RCDGs in BLCA, which provided the foundation for subsequent experiments and therapeutic options.

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“…However, this strategy has demonstrated numerous limits, and the emergence of drug resistance rendering tumors insensitive to apoptosis is crucial [ 15 ]. In this scenario, the discovery of drugs that induce nonapoptotic RCD is an intriguing approach for anticancer therapy, and compounds inducing NEC in tumors, including prostate cancer (PCa), are interesting [ 16 , 17 , 18 ].…”

Section: Introductionmentioning

confidence: 99%

“…CRPC patients among all PCa patients, and their poor prognosis and survival reflect the need to develop other drugs. Thus, the discovery of new antitumor drugs and active medical interventions on CRPC patients is urgent, and compounds that induce NEC are expected to produce benefits [ 17 , 21 ].…”

Section: Introductionmentioning

confidence: 99%

Necroptosis and Prostate Cancer: Molecular Mechanisms and Therapeutic Potential

Beretta

Zaffaroni

2022

Cells

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Necroptosis is a programmed form of necrosis characterized by mitochondrial alterations and plasma membrane permeabilization resulting in the release of cytoplasmic content into extracellular space, and leading to inflammatory reactions. Besides its critical role in viral defense mechanisms and inflammatory diseases, necroptosis plays pivotal functions in the drug response of tumors, including prostate cancer. Necroptosis is mainly governed by kinase enzymes, including RIP1, RIP3, and MLKL, and conversely to apoptosis, is a caspase-independent mechanism of cell death. Numerous compounds induce necroptosis in prostate cancer models, including (i) compounds of natural origin, (ii) synthetic and semisynthetic small molecules, and (iii) selenium and selenium-based nanoparticles. Here, we overview the molecular mechanisms underlying necroptosis and discuss the possible implications of drugs inducing necroptosis for prostate cancer therapy.

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Regulated Cell Death in Urinary Malignancies

Cited by 15 publications

References 186 publications

spARC recovers human glioma spatial signaling networks with graph filtering

spARC recovers human glioma spatial signaling networks with graph filtering

The Cross-talk, Genetic Alteration, Molecular Functions, and Cluster Relevance of the Major Types of Regulated Cell Death in Bladder Cancer

Necroptosis and Prostate Cancer: Molecular Mechanisms and Therapeutic Potential

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