Summary of project PR000388
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 PR000388. The data can be accessed directly via it's Project DOI: 10.21228/M8WP4C This work is supported by NIH grant, U2C- DK119886.
See: https://www.metabolomicsworkbench.org/about/howtocite.php
| Project ID: | PR000388 |
| Project DOI: | doi: 10.21228/M8WP4C |
| Project Title: | Regulation of Metabolism by LSR |
| Project Type: | LC-MS Lipidomics |
| Project Summary: | Breast cancer is a global crisis, accounting for nearly one quarter of all cancers in women. In the U.S., African-American (AA) women suffer disproportionately from breast cancer mortality compared to other racial/ethnic groups. Both social (socioeconomic factors, diet, obesity) and biological hypotheses (gene polymorphisms, gene expression profiling) have been advanced to explain these discrepancies, but the differences remain poorly understood. Multiple aspects of tumor aggressiveness have been identified in the AA population, including a high proportion of basal-like tumors. Basal-like tumors are clinically the most aggressive, characterized by enhanced cancer stem cell-like features. Currently, no effective molecular therapies exist for these highly aggressive cancers and patient survival is poor. Escalating this disparity is the disease promoting effects of obesity and metabolic syndrome, which are significantly higher in AA women. Obesity and its associated inflammation have been attributed to poor patient outcomes, resistance to chemotherapeutics, and/or cancer risk. A meta-analysis of 43 studies of obesity and breast cancer revealed that obese patients were 33% more likely than non-obese patients to die of breast cancer. Yet apart from correlative studies, no reports have combined these factors with cancer disparities to ascertain their molecular interactions and physiology on breast tumorigenesis. We tested the integration these factors, with focus on a specific molecule, Lipolysis Stimulated Lipoprotein Receptor (LSR), in the promotion of aggressive cancer behaviors. LSR is a cell surface molecule that regulates post-prandial lipid uptake in the liver, is sensitive to high fat diets, and is regulated by metabolic cues, including leptin. By testing each of these factors as well as their dynamic interactions on breast cancer tumorigenesis, we will gain valuable insight into biological mechanisms that influence cancer risk/disparities, response to therapy, and ultimately patient outcome. We recently reported LSR is overexpressed in breast tumors, directs aggressive breast cancer cell behaviors including proliferation and migration, and enhances cancer stem cell-like and chemotherapeutic resistance features in breast cancer cells. |
| Institute: | North Carolina Central University |
| Department: | Department of Biology |
| Last Name: | Fleming |
| First Name: | Jodie |
| Address: | 1801 Fayetteville Street, Durham, NC 27707 |
| Email: | Jodie.Fleming@nccu.edu |
| Phone: | 9195416861 |
Summary of all studies in project PR000388
| Study ID | Study Title | Species | Institute | Analysis(* : Contains Untargted data) | Release Date | Version | Samples | Download(* : Contains raw data) |
|---|---|---|---|---|---|---|---|---|
| ST000528 | Regulation of Metabolism by LSR | Homo sapiens | University of North Carolina | MS* | 2018-02-07 | 1 | 26 | Uploaded data (1.8G)* |
| ST000529 | Regulation of Metabolism by LSR (part II) | Homo sapiens | University of North Carolina | MS* | 2018-02-07 | 1 | 18 | Uploaded data (24.9G)* |
