Summary of Study ST002255

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 PR001346. The data can be accessed directly via it's Project DOI: 10.21228/M8QX47 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.

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Study IDST002255
Study TitleFunctional metabolic molecules were identified as novel therapeutic targets to facilitate gemcitabine treatment against pancreatic cancer (Cells metabolomics with ATP)
Study SummaryWith the development of frontier technologies in system biology, traditional omics-drove phenotypic studies are insufficient to decipher the diseases. Therefore, for a thorough understanding of the molecular mechanisms of diseases to investigate novel drug targets, traditional phenotypic studies must be broken through to the functional exploration of molecules. Meanwhile, the intuitive role of small molecule compounds (metabolites) in pathogenesis, precision diagnosis and therapy are gradually recognized compared to macromolecules such as DNA, RNA and proteins. Therefore, we pioneeringly proposed Spatial Temporal Operative Real Metabolomics (STORM) strategy that established a relationship between metabolic phenotypes and functions to accurately character abnormal metabolisms and further identify operative functional molecules as novel therapeutic targets. Here, given the difficulty of pancreatic cancer (PC) treatment and the high resistance of clinical drugs, we were committed to explore new targets and drugs of pancreatic cancer from a small molecular functional perspective via STORM strategy. Fortunately, based on targeted metabolomics, we found that gemcitabine, one of the most effective clinical anti-PC drugs, served as a dual modulator that promote the accumulation of functional metabolic molecules in purine metabolism to activate down-streamed kinases. And the quantitative consequences of related enzymes annotated the unique molecular mechanisms of purine metabolism regulations by gemcitabine. Collectively, we broadened the cognitions of gemcitabine in tumor inhibition, providing potential strategies for treating PC with small molecules modification. Even more importantly, with the integration of multiple frontier technologies, the STORM strategy has proven to be well adapted to the phenotypic era of functional molecules devoted to innovate molecule mechanism annotation and therapeutic discovery.
Institute
Shanghai Center for Systems Biomedicine, Shanghai Jiaotong University
DepartmentShanghai Center for Systems Biomedicine
LaboratoryLu Group
Last NameLu
First NameHaitao
Address800 Dongchuan RD. Minhang District, Shanghai, Shanghai, 200240, China
Emailjingjing2018@sjtu.edu.cn
Phone18818211315
Submit Date2022-08-04
Raw Data AvailableYes
Raw Data File Type(s)d
Analysis Type DetailLC-MS
Release Date2022-08-22
Release Version1
Haitao Lu Haitao Lu
https://dx.doi.org/10.21228/M8QX47
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

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Factors:

Subject type: Cultured cells; Subject species: Homo sapiens (Factor headings shown in green)

mb_sample_id local_sample_id Treatment
SA217097ASPC-CATP-125µl DMSO and 40µM ATP for 72h
SA217098ASPC-CATP-525µl DMSO and 40µM ATP for 72h
SA217099ASPC-CATP-425µl DMSO and 40µM ATP for 72h
SA217100ASPC-CATP-225µl DMSO and 40µM ATP for 72h
SA217101ASPC-CATP-325µl DMSO and 40µM ATP for 72h
SA217102ASPC-GATP-550µM gemcitabine and 40µM ATP for 72h
SA217103ASPC-GATP-450µM gemcitabine and 40µM ATP for 72h
SA217104ASPC-GATP-1-r00250µM gemcitabine and 40µM ATP for 72h
SA217105ASPC-GATP-250µM gemcitabine and 40µM ATP for 72h
SA217106ASPC-GATP-350µM gemcitabine and 40µM ATP for 72h
Showing results 1 to 10 of 10
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