Summary of Study ST004032
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 PR002524. The data can be accessed directly via it's Project DOI: 10.21228/M8CZ4G 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 | ST004032 |
| Study Title | SIRT3 induces cell senescence via regulating deacetylation of SLC25A13 in colorectal cancer |
| Study Type | research |
| Study Summary | In previous studies, we found that SIRT3 knockout can lead to mitochondrial dysfunction and induce mitochondrial dysfunction-associated cellular senescence. To further validate the impact of SIRT3 on colorectal cancer cell metabolism, in this study, we constructed shSIRT3 cells and NC (negative control) cells. By comparing the metabolic alterations between the two groups, we analyzed the regulatory role of SIRT3 in metabolic pathways. |
| Institute | Sichuan University |
| Department | Cancer Center and State Key Laboratory of Biotherapy |
| Laboratory | Cancer Center and State Key Laboratory of Biotherapy, |
| Last Name | WEI |
| First Name | LIU |
| Address | Linyin street, Chengdu, sichuan province, 610041, China |
| lwwl1995@163.com | |
| Phone | 18030469801 |
| Submit Date | 2025-07-09 |
| Raw Data Available | Yes |
| Raw Data File Type(s) | cdf, qgd |
| Analysis Type Detail | LC-MS |
| Release Date | 2025-07-31 |
| Release Version | 1 |
Select appropriate tab below to view additional metadata details:
Project:
| Project ID: | PR002524 |
| Project DOI: | doi: 10.21228/M8CZ4G |
| Project Title: | SIRT3 induces cell senescence via regulating deacetylation of SLC25A13 in colorectal cancer |
| Project Type: | research |
| Project Summary: | We demonstrate that SIRT3 knockdown induces mitochondrial dysfunction-associated senescence (MiDAS) in colorectal cancer (CRC) cells. Mechanistically, hyperacetylation of SLC25A13—a SIRT3 substrate—compromises its function, leading to a reduced cytosolic NAD+/NADH ratio and subsequent senescence. Furthermore, employing a 'hit-and-run' screening strategy, we identified senolytic agents capable of selectively eliminating senescent tumor cells, providing potential therapeutic avenues for CRC treatment |
| Institute: | Sichuan University |
| Department: | Cancer Center and State Key Laboratory of Biotherapy |
| Laboratory: | Cancer Center and State Key Laboratory of Biotherapy |
| Last Name: | WEI |
| First Name: | LIU |
| Address: | Linyin street, Chengdu, sichuan province, 610041, China |
| Email: | lwwl1995@163.com |
| Phone: | 18030469801 |
Subject:
| Subject ID: | SU004178 |
| Subject Type: | Cultured cells |
| Subject Species: | Homo sapiens |
| Taxonomy ID: | 9606 |
| Gender: | Not applicable |
Factors:
Subject type: Cultured cells; Subject species: Homo sapiens (Factor headings shown in green)
| mb_sample_id | local_sample_id | Genotype | treatment | Sample source |
|---|---|---|---|---|
| SA465498 | ShSIRT31-neg | SIRT3-knockdown | NAM | Colorectal cell |
| SA465499 | ShSIRT31-pos | SIRT3-knockdown | NAM | Colorectal cell |
| SA465500 | ShSIRT32-neg | SIRT4-knockdown | NAM | Colorectal cell |
| SA465501 | ShSIRT32-pos | SIRT4-knockdown | NAM | Colorectal cell |
| SA465502 | ShSIRT33-pos | SIRT5-knockdown | NAM | Colorectal cell |
| SA465503 | ShSIRT33-neg | SIRT5-knockdown | NAM | Colorectal cell |
| SA465504 | ShSIRT34-pos | SIRT6-knockdown | NAM | Colorectal cell |
| SA465505 | ShSIRT34-neg | SIRT6-knockdown | NAM | Colorectal cell |
| SA465506 | ShSIRT35-pos | SIRT7-knockdown | NAM | Colorectal cell |
| SA465507 | ShSIRT35-neg | SIRT7-knockdown | NAM | Colorectal cell |
| SA465508 | ShSIRT36-pos | SIRT8-knockdown | NAM | Colorectal cell |
| SA465509 | ShSIRT36-neg | SIRT8-knockdown | NAM | Colorectal cell |
| SA465510 | NC5-pos | wild-type | control | Colorectal cell |
| SA465511 | NC6-pos | wild-type | control | Colorectal cell |
| SA465512 | NC1-neg | wild-type | control | Colorectal cell |
| SA465513 | NC4-pos | wild-type | control | Colorectal cell |
| SA465514 | NC3-pos | wild-type | control | Colorectal cell |
| SA465515 | NC2-pos | wild-type | control | Colorectal cell |
| SA465516 | NC2-neg | wild-type | control | Colorectal cell |
| SA465517 | NC6-neg | wild-type | control | Colorectal cell |
| SA465518 | NC5-neg | wild-type | control | Colorectal cell |
| SA465519 | NC4-neg | wild-type | control | Colorectal cell |
| SA465520 | NC3-neg | wild-type | control | Colorectal cell |
| SA465521 | NC1-pos | wild-type | control | Colorectal cell |
| Showing results 1 to 24 of 24 |
Collection:
| Collection ID: | CO004171 |
| Collection Summary: | Additionally, to ensure data quality for metabolic profiling, Quality control (QC) samples were prepared by pooling aliquots of all samples that were representative of the all samples under analysis, and used for data normalization. QC samples were prepared and analyzed with the same procedure as that for the experiment samples in each batch. Dried extracts were then dissolved in 50% acetonitrile. Each sample was filtered with a disposable 0.22 µm cellulose acetate and transferred into 2 mL HPLC vials and stored at -80℃ until analysis. |
| Sample Type: | colorectal cell |
Treatment:
| Treatment ID: | TR004187 |
| Treatment Summary: | RKO cells were stably-transfected with NC and shSIRT3, and NC and transfected cells were treated with 10 mM nicotinamide (Nico) for 6 h followed by 72 h pyruvate deprivation. |
Sample Preparation:
| Sampleprep ID: | SP004184 |
| Sampleprep Summary: | Metabolomics profiling was analyzed using a UPLC-ESI-Q-Orbitrap-MS system (UHPLC, Shimadzu Nexera X2 LC-30AD， Shimadzu，Japan) coupled with Q-Exactive Plus (Thermo Scientific, San Jose, USA). For liquid chromatography (LC) separation, samples were analyzed using a ACQUITY UPLC® HSS T3 column (2.1 × 100 mm, 1.8 μm）(Waters, Milford, MA, USA). The flow rate was 0.3 mL/min and the mobile phase contained: A: 0.1% FA in water and B: 100% acetonitrile (ACN). The gradient was 0% buffer B for 2 min and was linearly increase to 48% in 4 min, and then up to 100% in4 min and maintained for 2 min, and then decreased to 0% buffer B in 0.1 min, with 3 min re-equilibration period employed. The electrospray ionization (ESI) with positive-mode and negative mode were applied for MS data acquisition separately. The HESI source conditions were set as follows: Spray Voltage：3.8kv (positive) and 3.2kv (negative)；Capillary Temperature：320℃; Sheath Gas (nitrogen) flow: 30 arb (arbitrary units); Aux Gas flow: 5 arb; Probe Heater Temp: 350℃; S-Lens RF Level：50. The instrument was set to acquire over the m/z range 70-1050 Da for full MS. The full MS scans were acquired at a resolution of 70,000 at m/z 200, and 17,500 at m/z 200 for MS/MS scan. The maximum injection time was set to for 100 ms for MS and 50 ms for MS/MS. The isolation window for MS2 was set to 2 m/z and the normalized collision energy (stepped) was set as 20, 30 and 40 for fragmentation. |
Chromatography:
| Chromatography ID: | CH005066 |
| Instrument Name: | Waters Acquity |
| Column Name: | Waters ACQUITY UPLC HSS T3 (100 x 2.1 mm, 1.8 μm) |
| Column Temperature: | 37℃ |
| Flow Gradient: | The gradient was 0% buffer B for 2 min and was linearly increase to 48% in 4 min, and then up to 100% in4 min and maintained for 2 min, and then decreased to 0% buffer B in 0.1 min, with 3 min re-equilibration period employed |
| Flow Rate: | 0.3 mL/min |
| Solvent A: | 100% Water; 0.1% Formic acid |
| Solvent B: | 100% Acetonitrile |
| Chromatography Type: | Reversed phase |
Analysis:
| Analysis ID: | AN006668 |
| Analysis Type: | MS |
| Chromatography ID: | CH005066 |
| Num Factors: | 7 |
| Num Metabolites: | 212 |
| Units: | peak intensity |
| Analysis ID: | AN006669 |
| Analysis Type: | MS |
| Chromatography ID: | CH005066 |
| Num Factors: | 7 |
| Num Metabolites: | 212 |
| Units: | peak intensity |
