PXD002736 is an
original dataset announced via ProteomeXchange.
Dataset Summary
Title | Quantitative phosphoproteomics analysis uncovers the regulatory networks of minichromosome maintenance protein 2 in lung cancer cells |
Description | Minichromosome maintenance protein 2 (MCM2) is a licensing factor for DNA replication. It interacts with other MCM proteins to comprise MCM2-7 complex, which acts as a helicase for DNA unwinding and limits DNA replication to one round per cell cycle. MCM2 has been widely used as a biomarker for proliferation in many types of cancer. However, the molecular regulation underlying MCM2 in lung cancer cells is poorly understood. In this study, we investigated the role of MCM2 in lung adenocarcinoma A549 (wild-type p53) and H1299 (null p53) cells. MCM2 overexpression increased cell proliferation in A549 cells while silencing MCM2 decreased cell proliferation in H1299 cells. We performed global quantitative phosphoproteomic analysis to uncover the important downstream networks regulated by MCM2 in lung cancer cells. We identified 1484 phosphorylation sites in 593 phosphoproteins of MCM2-overexpressed A549 cells. Of these phosphosites, 110 phosphoproteins were significantly changed in response to MCM2 overexpression. In addition, we identified 1599 phosphorylation sites in 592 phosphoproteins of MCM2-silenced H1299 cells. Of these phosphosites, 57 phosphoproteins were significantly changed in response to MCM2 silencing. The differentially regulated phosphoproteins are involved in biological functions such as RNA splicing, cell cycle and cytoskeleton regulation. Functional study demonstrated that MCM2 overexpression promoted cell migration in A549 cells. Moreover, silencing MCM2 inhibits cell migration and induces cell cycle arrest in H1299 cells. Furthermore, we observed a common phosphorylation change at Ser-99 of high mobility group protein HMG-I/HMG-Y (HMGA1) in both MCM2 overexpression and silencing, indicating an important regulatory effect of Ser-99 HMGA1 on lung cancer cells. The phosphoproteomic profiling of MCM2 in lung cancer cells provides new insight about phosphorylation networks regulated by MCM2 and reveals novel targets for lung cancer therapy. |
HostingRepository | PRIDE |
AnnounceDate | 2024-10-22 |
AnnouncementXML | Submission_2024-10-22_04:02:32.355.xml |
DigitalObjectIdentifier | |
ReviewLevel | Peer-reviewed dataset |
DatasetOrigin | Original dataset |
RepositorySupport | Unsupported dataset by repository |
PrimarySubmitter | Siao Chong |
SpeciesList | scientific name: Homo sapiens (Human); NCBI TaxID: 9606; |
ModificationList | phosphorylated residue; monohydroxylated residue |
Instrument | LTQ Orbitrap |
Dataset History
Revision | Datetime | Status | ChangeLog Entry |
0 | 2015-08-17 01:48:25 | ID requested | |
1 | 2018-10-24 10:52:05 | announced | |
⏵ 2 | 2024-10-22 04:02:38 | announced | 2024-10-22: Updated project metadata. |
Publication List
10.1038/s41598-017-13440-x; |
Cheung CHY, Hsu CL, Chen KP, Chong ST, Wu CH, Huang HC, Juan HF, MCM2-regulated functional networks in lung cancer by multi-dimensional proteomic approach. Sci Rep, 7(1):13302(2017) [pubmed] |
Keyword List
curator keyword: Biomedical |
submitter keyword: lung cancer cells, minichromosome maintenance protein-2, regulatory networks,Quantitative phosphoproteome |
Contact List
Hsueh-Fen Juan, Ph.D. |
contact affiliation | Institute of Molecular and Cellular Biology, National Taiwan University, Taipei, Taiwan. Department of Life Science, National Taiwan University, Taipei, Taiwan. Department of Electrical Engineering, National Taiwan University, Taipei, Taiwan |
contact email | yukijuan@ntu.edu.tw |
lab head | |
Siao Chong |
contact affiliation | National Taiwan University |
contact email | choonghua89@gmail.com |
dataset submitter | |
Full Dataset Link List
Dataset FTP location
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PRIDE project URI |
Repository Record List
[ + ]
[ - ]
- PRIDE
- PXD002736
- Label: PRIDE project
- Name: Quantitative phosphoproteomics analysis uncovers the regulatory networks of minichromosome maintenance protein 2 in lung cancer cells