Summary of project PR002704
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 PR002704. The data can be accessed directly via it's Project DOI: 10.21228/M84K1C This work is supported by NIH grant, U2C- DK119886.
See: https://www.metabolomicsworkbench.org/about/howtocite.php
| Project ID: | PR002704 |
| Project DOI: | doi: 10.21228/M84K1C |
| Project Title: | Exploring the Impact of Doxorubicin and Paclitaxel on HCT-116 Cancer Cells: A Comprehensive Multi-Omics Analysis Using Mass Spectrometry |
| Project Summary: | Background: Colorectal cancer is the second leading cause of cancer-related mortality worldwide and ranks as the third most prevalent cancer in the United Arab Emirates. CRC presents a formidable challenge due to its high metastatic potential and limited treatment options. This study investigates the effects of paclitaxel and doxorubicin on the HCT-116 cancer cell line, utilizing a multi-omics approach to identify molecular alterations induced by these treatments. Methodology: Metabolomics and proteomics analysis were employed on HCT-116 cells treated with paclitaxel, doxorubicin, and a combination of both agents. Analyses were conducted using TIMS-QTOF-UHPLC-MS, with four biological replicates per treatment condition. Results: Following a two-tailed independent Student’s t-test with q-value <0.05, paclitaxel treatment yielded 9 altered metabolites and 46 dysregulated proteins, while doxorubicin treatment resulted in 9 metabolites and 238 dysregulated proteins. The combination therapy led to the dysregulation of 19 metabolites and 308 proteins. Enrichment analysis highlighted significant effects on purine metabolism by both treatments, with doxorubicin also impacting citric acid and gluconeogenesis pathways. Paclitaxel uniquely influenced spermidine and spermine biosynthesis, whereas combined treatment showed an additive impact on amino acid metabolism, including alterations in aspartate, proline, and arginine pathways. Both compounds were observed to deactivate RNA processing, translation, and ribosome biogenesis, effectively impairing protein synthesis and reducing cancer cell proliferation and survival. Conclusion: Paclitaxel and doxorubicin induce distinct metabolic and proteomic alterations in CRC cells, impacting critical pathways for cancer survival. Combined therapy offers enhanced disruption of amino acid metabolism, highlighting its potential for improved therapeutic efficacy in CRC treatment. |
| Institute: | Sharjah Institute for Medical Research |
| Last Name: | Facility |
| First Name: | Core |
| Address: | M32, SIMR, College of Pharmacy, Health Sciences, University of Sharjah, Sharjah, UAE, Sharjah, 000, United Arab Emirates |
| Email: | tims-tof@sharjah.ac.ae |
| Phone: | +971 6 5057656 |
Summary of all studies in project PR002704
| Study ID | Study Title | Species | Institute | Analysis(* : Contains Untargted data) | Release Date | Version | Samples | Download(* : Contains raw data) |
|---|---|---|---|---|---|---|---|---|
| ST004280 | Exploring the Impact of Doxorubicin and Paclitaxel on HCT-116 Cancer Cells: A Comprehensive Multi-Omics Analysis Using Mass Spectrometry | Homo sapiens | Sharjah Institute for Medical Research | MS | 2025-11-03 | 1 | 32 | Uploaded data (8.6G)* |
