Summary of Study ST003639
This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR002250. The data can be accessed directly via it's Project DOI: 10.21228/M8SJ9Z This work is supported by NIH grant, U2C- DK119886.
See: https://www.metabolomicsworkbench.org/about/howtocite.php
This study contains a large results data set and is not available in the mwTab file. It is only available for download via FTP as data file(s) here.
| Study ID | ST003639 |
| Study Title | Multilevel Plasticity and Altered Glycosylation Drive Aggressiveness in Hypoxic and Glucose-Deprived Bladder Cancer Cells |
| Study Type | MS quantitative analysis |
| Study Summary | 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. |
| Institute | Portuguese Oncology Institute of Porto (IPO-Porto) |
| Department | IPO Porto Research Center |
| Laboratory | Lab 2 |
| Last Name | Peixoto |
| First Name | Andreia |
| Address | Rua Dr. António Bernardino de Almeida |
| andreia.peixoto@ipoporto.min-saude.pt | |
| Phone | 225084000 (ext:5111) |
| Submit Date | 2024-12-18 |
| Raw Data Available | Yes |
| Raw Data File Type(s) | raw(Thermo) |
| Analysis Type Detail | LC-MS |
| Release Date | 2025-01-20 |
| Release Version | 1 |
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Factors:
Subject type: Cultured cells; Subject species: Homo sapiens (Factor headings shown in green)
| mb_sample_id | local_sample_id | Sample source | Treatment |
|---|---|---|---|
| SA394027 | 5637_H1 | 5637 cells | Hypoxia plus glucose restriction |
| SA394028 | 5637_H2 | 5637 cells | Hypoxia plus glucose restriction |
| SA394029 | 5637_H3 | 5637 cells | Hypoxia plus glucose restriction |
| SA394030 | 5637_N1 | 5637 cells | Normoxia |
| SA394031 | 5637_N2 | 5637 cells | Normoxia |
| SA394032 | 5637_N3 | 5637 cells | Normoxia |
| SA394033 | T24_H1 | T24 cells | Hypoxia plus glucose restriction |
| SA394034 | T24_H2 | T24 cells | Hypoxia plus glucose restriction |
| SA394035 | T24_H3 | T24 cells | Hypoxia plus glucose restriction |
| SA394036 | T24_N1 | T24 cells | Normoxia |
| SA394037 | T24_N2 | T24 cells | Normoxia |
| SA394038 | T24_N3 | T24 cells | Normoxia |
| Showing results 1 to 12 of 12 |
