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Intracellular Interleukin-1α in Peritumoral Monocytes Induces IL8 Production and Inhibits Mitophagy to Promote Stemness and Metastasis of Hepatocellular Carcinoma

ABSTRACT: Intracellular Interleukin-1α in Peritumoral Monocytes Induces IL8 Production and Inhibits Mitophagy to Promote Stemness and Metastasis of Hepatocellular Carcinoma

PROVIDER: PRJNA1203603 | ENA |

REPOSITORIES: ENA

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Intracellular Interleukin-1α in Peritumoral Monocytes Induces IL8 Production and Inhibits Mitophagy to Promote Stemness and Metastasis of Hepatocellular Carcinoma

Project description:In the current study, we found that IL-1α levels were significantly upregulated in peritumoral monocytes compared to nontumor and intratumor counterparts, and glycolytic switch mediated the upregulation of IL-1α via NF-κB signaling. The upregulated IL-1α was neither secreted by nor displayed on cell surface of monocytes. Rather, IL-1α translocated into nuclei to induce the production of IL-8, which effectively enhanced cancer cell stemness and tumor metastasis. Substantial amounts of IL-1α bound to mitochondria to inhibit mitophagy, inducing CA12 expression and macrophages accumulation via ROS-HIF-1α pathway. In accordance, IL-1α levels in peritumoral monocytes were positively correlated with both survival and tumor metastasis of HCC patients. Targeting IL-1α+ monocytes or IL-8 could effectively inhibited tumor progression and enhanced tumor responsiveness to immune checkpoint blockade therapy in mice in vivo. Our results revealed an intracellular regulatory role of IL-1α in modifying the pro-tumor functions of monocytes within specific tumor microenvironments, and pointed to both IL-1α and its downstream IL-8 as potential diagnostic and therapeutic targets for human HCC.

2025-08-01 | GSE285415 | GEO

Genome-wide analysis of PGC-1α-binding in microglia

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The global IL-1α gene expression response in p65 enhancer mutant HeLa cells.

Project description:Conversion of cytokine-driven changes in chromatin topology into gene regulatory circuits during inflammation still remains unclear. Here, we analyzed the expression profiles of HeLa cells carrying microdeletions of p65-binding sites in two enhancers regulating the IL-1α-inducible IL8 and CXCL1-3 genes within the extended chemokine locus on human chromosome 4.

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Expression data of FFPE peritumoral neocortex tissue

Project description:Epilepsy is a common cause of morbidity affecting approximately one third of patients with primary brain tumors. However, the molecular mechanism underlying the tumor induced epileptogenesis is poorly understood. The alteration in peritumoral microenvironments is believed to play a significant role in inducing epileptogenesis. We hypothesize that the change of gene expression in neighboring astrocytes and neurons may contribute to the increased neuronal excitability and epileptogenesis. Genome-wide gene expression profiling was conducted using Affymetrix HG U133 plus 2.0 arrays and RNAs derived from formalin-fixed paraffin embedded (FFPE) peritumoral cortex tissue slides from 5-paired (seizure vs. non-seizure) low grade brain tumor patients.

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Host-derived Interleukin 1α induces immune suppressive tumor microenvironment via regulation of monocyte-to-macrophage differentiation

Project description:Tumor-associated macrophages exhibit high heterogeneity and contribute to the establishment of an immune-suppressive tumor microenvironment (TME). Although numerous studies have demonstrated that extracellular factors promote macrophage proliferation and polarization, the regulatory mechanisms governing the differentiation process to generate phenotypically, and functionally diverse macrophage subpopulations remain largely unexplored. In this study, we examined the influence of interleukin 1α (IL-1α) on the development of an immune-suppressive TME using syngeneic transplantation murine models of breast cancer. Deletion of IL-1α led to the rejection of syngeneic tumor challenges. Single-cell sequencing analysis revealed that Cx3cr1+ macrophage cells were the primary sources of IL-1α in the TME. The absence of IL-1α reprogrammed the monocyte-to-macrophage differentiation process within the TME, characterized by a notable decrease in the subset of Cx3cr+ ductal-like macrophages and an increase in iNos-expressing stress-responsive cells. Comparative analysis of gene signatures in both human and mouse macrophage subsets suggested that IL-1α deficiency shifted macrophage polarization from M2 to M1 phenotypes, leading to enhanced cytotoxic T lymphocyte activity in the TME. Importantly, elevated levels of IL-1α in human cancers were associated with improved prognosis following immunotherapy. These findings underscore the pivotal role of IL-1α in shaping an immune-suppressive TME through the regulation of macrophage differentiation and activity, highlighting IL-1α as a potential target for breast cancer immunotherapy.

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MiRNome profiling of glioblastoma tissues and peritumoral regions

Project description:Glioblastoma multiforme (GBM) is the most common and deadliest primary brain tumor. Its prognosis is inexorably unfavorable, as these tumors drive affected patients to death usually within 15 months after diagnosis (short term survivors, ST), with the only exception of a small fraction of patients (long term survivors, LT) surviving longer than 36 months. Even after the frontline therapeutic approach, including surgical resection followed by chemo- and radiotherapy, the cause of death in most cases is tumor recurrence, which occurs in peritumoral tissues in about 95% of patients. Here, we provide a comprehensive molecular analysis of a set of ST and LT samples derived from frankly tumoral areas (C) and from the peritumoral regions (P) of the same patients. By performing microRNA deep sequencing, we collected data showing that P areas differ from healthy white matter, but share with C samples, a number of microRNAs

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CD160+ NK cells from intratumoral and peritumoral tissues

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Functional switching of the peritumoral cutaneous Schwann cells in melanoma

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