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Paradoxical drug sensitization of lung cancer cells by stromal fibroblast-secreted IGF-binding proteins

ABSTRACT: Paradoxical drug sensitization of lung cancer cells by stromal fibroblast-secreted IGF-binding proteins

PROVIDER: PRJNA691893 | ENA |

REPOSITORIES: ENA

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Paradoxical drug sensitization of lung cancer cells by stromal fibroblast-secreted IGF-binding proteins: Secretomics

Project description:Cancer-associated fibroblasts (CAFs) are an integral part of the tumor microenvironment often linked to drug resistance. Here, we report that CAFs, but not normal fibroblasts, can promote either resistance or unexpected drug sensitization of different lung cancer cells. Using unbiased secretomics, transcriptomics and tyrosine phosphoproteomics, we observed differential expression of several IGF1R signaling components, such as IGF-binding proteins and IGF1/2, and downstream signaling effects on cancer cells by fibroblasts. IGF1/2 treatment or IGFBP5 silencing in CAFs reversed, while addition of exogenous IGFBPs or pharmacological IGF1R inhibitors phenocopied the sensitizing effects. Combining IGF1R and EGFR inhibitors synergized in 2D and 3D models of different drug-resistant and naïve EGFR-mutant lung cancer cells and decreased tumor growth in vivo. These results suggest that multiple resistance mechanisms coexist within the same cancer cells, that CAFs context-dependently cause drug resistance or sensitization, and that understanding both of these differential mechanisms leads to improved therapeutic approaches.

2023-03-11 | PXD023626 | Pride

Paradoxical drug sensitization of lung cancer cells by stromal fibroblast-secreted IGF-binding proteins: Phosphotyrosine Profiling

2023-03-11 | PXD023692 | Pride

Paradoxical drug sensitization of lung cancer cells by stromal fibroblast-secreted IGF-binding proteins

Project description:Cells were grown to 80-90% confluency before RNA extraction. Microarray-measured basal gene expression was used to differentiate the various cell types, e.g., CAFs vs NAFs.

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LC-MS/MS analysis of human brain fibroblast-secreted molecules

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Transcriptomic Predictors of Paradoxical Cryptococcosis-Associated Immune Reconstitution Inflammatory Syndrome

Project description:Paradoxical cryptococcosis-associated immune reconstitution inflammatory syndrome

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Neurotrophic factors and their receptors are altered by the mere partial IGF-1 deficiency

Project description:Neurotrophic factors (NTFs) are a relevant group of secreted proteins that modulate growth, differentiation, repair, and survival of neurons; playing a role in the maintenance of the synaptic unions, dendrites and axons; also, being crucial for peripheral nervous system development and regulating plasticity in the adult central nervous system. On the other hand, insulin-like growth factor 1 (IGF-1) has been ascertained multiple beneficial actions in the brain: neuro-development, -protection, -genesis and plasticity. To further investigate the possible mechanisms underlying IGF-1 deficiency in the establishment of neurological disease, microarray and RT-qPCR gene expression analyses coupled with in silico processing were performed in an experimental model of partial IGF-1 deficiency. Results show that the mere IGF-1 deficiency seems to be responsible for an altered expression of genes coding for neurotrophic factors (particularly ciliary neurotrophic factor and mesencephalic astrocyte-derived neurotrophic factor), their receptors and signaling pathways (specially RET). The presented findings support that IGF-1 deficiency might be involved in the establishment and progression of neurodegenerative disorders.

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Expression data from Igf-1 -/- and Igf-1+/+ mouse cochleas

Project description:Different mutations in the gene encoding humans IGF-I cause intrauterine growth retardation, postnatal growth failure, microcephaly, mental retardation, bilateral sensorineural deafness and multiple dysmorphic features. Insight into the role of IGFs in inner ear cochlear ganglion neurogenesis has come from the study of genetically modified mice. Postnatal cochlear development is severely impaired in mice Igf1-/-, which develop smaller cochlea and cochlear ganglia, an immature tectorial membrane and they display a significant decrease in the number and size of auditory neurons. We used microarrays to define the genetic signatures of Igf-1 +/+ and Igf-1-/- mouse cochea and identify the differentially expressed genes. Keywords: comparison between WT and KO

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Cancer-Associated Fibroblast Secreted Collagen is associated with Immune Suppressive LAIR-1 in Gliomas

Project description:Cancer-Associated Fibroblast Secreted Collagen is associated with Immune Suppressive LAIR-1 in Gliomas

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Cancer-associated fibroblast-secreted FGF2 faliciates gastric cancer cell proliferation by enhancing ribosome biogenesis

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Circulating insulin-like growth factor (IGF)-1 Regulates Hippocampal IGF-1 Levels and Brain Gene Expression During Adolescence

Project description:This study, using a growth hormone (GH)-deficient dwarf animal model and peripheral GH replacement, investigated the effects of circulating IGF-1 during adolescence on IGF-1 levels in the brain. Our results demonstrated that hippocampal IGF-1 protein concentrations during adolescence are highly regulated by circulating IGF-1, which were reduced by GH deficiency and restored by systematic GH replacement. In contrast, IGF-1 levels in the CSF were decreased by GH deficiency but not restored by GH replacement. Furthermore, analysis of gene expression using microarrays and RT-PCR indicated that circulating IGF-1 levels did not modify the transcription of IGF-1 or its receptor in the hippocampus but did regulate genes that are involved in microvascular structure and function, brain development, and synaptic plasticity, which potentially support brain structures involved in cognitive function during this important developmental period.

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