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Multilevel Plasticity and Altered Glycosylation Drive Aggressiveness in Hypoxic and Glucose-Deprived Bladder Cancer Cells

ABSTRACT: Multilevel Plasticity and Altered Glycosylation Drive Aggressiveness in Hypoxic and Glucose-Deprived Bladder Cancer Cells

PROVIDER: PRJNA1199976 | ENA |

REPOSITORIES: ENA

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Multilevel Plasticity and Altered Glycosylation Drive Aggressiveness in Hypoxic and Glucose-Deprived Bladder Cancer Cells

Project description:Bladder tumours with aggressive characteristics often present microenvironmental niches marked by low oxygen levels (hypoxia) and limited glucose supply due to inadequate vascularization. The molecular mechanisms facilitating cellular adaptation to these stimuli remain largely elusive. Employing a multi-omics approach, we discovered that hypoxic and glucose-deprived cancer cells enter a quiescent state supported by mitophagy, fatty acid β-oxidation, and amino acid catabolism, concurrently enhancing their invasive capabilities. Reoxygenation and glucose restoration efficiently reversed cell quiescence without affecting cellular viability, highlighting significant molecular plasticity in adapting to microenvironmental challenges. Furthermore, cancer cells exhibited substantial perturbation of protein O-glycosylation, leading to simplified glycophenotypes with shorter glycosidic chains. Exploiting glycoengineered cell models, we established that immature glycosylation contributes to reduced cell proliferation and increased invasion. Our findings collectively indicate that hypoxia and glucose deprivation trigger cancer aggressiveness, reflecting an adaptive escape mechanism underpinned by altered metabolism and protein glycosylation, providing grounds for clinical intervention.

2025-02-12 | GSE284635 | GEO

Multilevel Plasticity and Altered Glycosylation Drive Aggressiveness in Hypoxic and Glucose-Deprived Bladder Cancer Cells

Project description:Bladder tumours with aggressive characteristics often inhabit microenvironmental niches marked by low oxygen levels (hypoxia) and limited glucose supply due to inadequate vascularization. The molecular mechanisms facilitating cellular adaptation to these stimuli remain largely elusive. Employing a multi-omics approach, we discovered that hypoxic and glucose-deprived cancer cells enter a quiescent state supported by mitophagy, fatty acid β-oxidation, and amino acid catabolism, concurrently enhancing their invasive capabilities remarkably. Reoxygenation and glucose restoration efficiently reversed cell dormancy without affecting cellular viability, highlighting significant molecular plasticity in adapting to microenvironmental cues. Furthermore, cancer cells exhibited substantial perturbation of protein O-glycosylation, leading to simplified glycophenotypes with shorter glycosidic chains. Exploiting glycoengineered cell models, we established that immature glycosylation contributes to reduced cell proliferation and increased invasion. Our findings collectively indicate that hypoxia and glucose deprivation trigger cancer aggressiveness, reflecting an adaptive escape mechanism underpinned by altered metabolism and protein glycosylation. Building on these data, we have performed on a phosphoproteomics characterization of hypoxic and glucose-deprived bladder cancer cell lines, aiming to gain a deeper understanding of the signaling rewiring experienced by cancer cells under microenvironmental stress and to identify potential targets for future clinical intervention.

2024-03-27 | PXD045777 | Pride

Depletion of MALAT1-dependent WTAP reduces aggressiveness of hypoxic TNBC cells

Project description:Depletion of MALAT1-dependent WTAP reduces aggressiveness of hypoxic TNBC cells

| PRJNA1004313 | ENA

Effect of DGAT loss on hypoxic tumor cells growing under serum-deprived conditions

Project description:Effect of DGAT loss on hypoxic tumor cells growing under serum-deprived conditions

| PRJNA483168 | ENA

P104 mouse non-deprived vs. deprived visual cortex

2006-02-24 | GSE4266 | GEO

P46 mouse non-deprived vs. deprived visual cortex

Project description:Wild-type (C57Bl6) mice underwent monocular enucleation at P42 and were sacrificed 4 days later at P46. Bilateral (non-deprived and deprived) visual cortex was dissected from 1-mm thick coronal sections, and total RNA was extracted from the tissue lysate using Trizol (Gibco-BRL). Keywords: repeat

2006-02-24 | GSE4265 | GEO

P24 mouse non-deprived vs. deprived visual cortex

Project description:Wild-type (C57Bl6) mice underwent monocular enucleation at P20 and were sacrificed 4 days later at P24. Bilateral (non-deprived and deprived) visual cortex was dissected from 1-mm thick coronal sections, and total RNA was extracted from the tissue lysate using Trizol (Gibco-BRL). Keywords: repeat

2006-02-24 | GSE4264 | GEO

P18 mouse non-deprived vs. deprived visual cortex

Project description:Wild-type (C57Bl6) mice underwent monocular enucleation at P14 and were sacrificed 4 days later at P18. Bilateral (non-deprived and deprived) visual cortex was dissected from 1-mm thick coronal sections, and total RNA was extracted from the tissue lysate using Trizol (Gibco-BRL). Keywords: repeat

2006-02-24 | GSE4263 | GEO

Candida Iron deprived Cells: Control vs. BPS treated

Project description:Transcriptional profiling of iron deprived Candida cells comparing the WT vs BPS (Iron deprived) cells

2010-11-17 | GSE25394 | GEO

Transcription profiling of mouse P104 non-deprived vs. deprived visual cortex

Project description:Wild-type (C57Bl6) mice underwent monocular enucleation at P100 and were sacrificed 4 days later at P104. Bilateral (non-deprived and deprived) visual cortex was dissected from 1-mm thick coronal sections, and total RNA was extracted from the tissue lysate using Trizol (Gibco-BRL). Experiment Overall Design: Gene expression in pooled samples from 3 non-deprived (ipsilateral to monocular enucleation) and 3 deprived (contralateral to monocular enucleation) visual hemispheres was compared.

2008-06-13 | E-GEOD-4266 | biostudies-arrayexpress

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