Summary of project PR002055
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 PR002055. The data can be accessed directly via it's Project DOI: 10.21228/M8052C This work is supported by NIH grant, U2C- DK119886.
See: https://www.metabolomicsworkbench.org/about/howtocite.php
| Project ID: | PR002055 |
| Project DOI: | doi: 10.21228/M8052C |
| Project Title: | Comparative analysis of breast cancer metabolomes highlights fascin's central role in regulating key pathways related to disease progression |
| Project Summary: | Omics technologies provide useful tools for the identification of novel biomarkers in many diseases, including breast cancer, which is the most diagnosed cancer in women worldwide. We and others have reported a central role for the actin-bundling protein (fascin) in regulating breast cancer disease progression at different levels. However, whether fascin expression promotes metabolic molecules that could predict disease progression has not been fully elucidated. Here, fascin expression was manipulated via knockdown (fascinKD+NORF) and rescue (fascinKD+FORF) in the naturally fascin-positive (fascinpos+NORF) MDA-MB-231 breast cancer cells. Whether fascin dysregulates metabolic profiles that are associated with disease progression was assessed using untargeted metabolomics analyses via liquid chromatography-mass spectrometry. An overall of 12,226 metabolites were detected in the tested cell pellets. Fascinpos+NORF cell pellets showed 2,510 and 3,804 significantly dysregulated metabolites compared to their fascinKD+NORF counterparts. Fascin rescue (fascinKD+FORF) revealed 2,710 significantly dysregulated cellular metabolites compared to fascinKD+NORF counterparts. 101 overlapped cellular metabolites between fascinKD+FORF and fascinpos+NORF were significantly dysregulated in the fascinKD+NORF cells. Analysis of the significantly dysregulated metabolites by fascin expression revealed their involvement in the metabolism of sphingolipid, phenylalanine, tyrosine and tryptophan biosynthesis, and pantothenate and CoA biosynthesis, which are critical pathways for breast cancer progression. Our findings of fascin-mediated alteration of metabolic pathways could be used as putative poor prognostic biomarkers and highlight other underlying mechanisms of fascin contribution to breast cancer progression. |
| Institute: | King Faisal Specialist Hospital and Research Centre (KFSHRC) |
| Last Name: | AlMalki |
| First Name: | Reem |
| Address: | Al Mather road, Riyadh, KSA, 11211, Saudi Arabia |
| Email: | rgalmalki@kfshrc.edu.sa |
| Phone: | +966534045397 |
Summary of all studies in project PR002055
| Study ID | Study Title | Species | Institute | Analysis(* : Contains Untargted data) | Release Date | Version | Samples | Download(* : Contains raw data) |
|---|---|---|---|---|---|---|---|---|
| ST003305 | Comparative analysis of breast cancer metabolomes highlights fascin's central role in regulating key pathways related to disease progression | Homo sapiens | King Faisal Specialist Hospital and Research Centre (KFSHRC) | MS* | 2024-07-30 | 1 | 22 | Uploaded data (36.2G)* |
