Proteomics

Dataset Information

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Global Proteomic Analysis of Ovarian Clear Cell Carcinoma Cells Lacking ARID1A Reveals Upregulated Mitochondrial Electron Transport Chain Activity


ABSTRACT: Ovarian clear cell carcinoma (OCCC) is the most lethal gynecological cancer. It is characterized by somatic inactivating mutations of ARID1A, a component of the SWI/SNF chromatin-remodeling complex, occurring in up to 70% of patients. Patients with these mutations in their tumors have considerably poorer outcomes compared to those without such mutations. ARID1A-deficient cells have been shown to have a higher dependence on mitochondrial respiration, suggesting that targeting mitochondrial respiration is a promising approach to eliminating ARID1A-deficient cancer cells. Here we generated and characterized OCCC-derived ARID1A wild type and knock-out cell lines. Our proteomic data provide evidence of the increased relative abundance of mETC proteins in the ARID1A knock-out OCCC cells. Taken together, our data provides a rationale for identifying therapeutic vulnerabilities within the mETC in the context of treating ARID1A-deficient OCCC.

INSTRUMENT(S): Q Exactive Plus

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture

DISEASE(S): Ovarian Clear Cell Carcinoma

SUBMITTER: Stefani Thomas  

LAB HEAD: Stefani N. Thomas

PROVIDER: PXD050332 | Pride | 2025-07-07

REPOSITORIES: Pride

Dataset's files

Source:
Action DRS
RMG1_WT-D9-G11_F1.raw Raw
RMG1_WT-D9-G11_F10.raw Raw
RMG1_WT-D9-G11_F11.raw Raw
RMG1_WT-D9-G11_F12.raw Raw
RMG1_WT-D9-G11_F2.raw Raw
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Publications

Proteomic Analysis of ARID1A-Deficient Ovarian Clear Cell Carcinoma Cells Reveals Differential Mitochondria ETC Subunit Abundances and Targetable Mitochondrial Pathways.

Perez Jesenia M JM   Ryu Joohyun J   Khan Hannah H   Shetty Mihir M   Parker Emma E   D'Arcy Padraig P   Zhu Shijia S   Bazzaro Martina M   Thomas Stefani N SN  

International journal of molecular sciences 20250607 12


ARID1A-deficient ovarian clear cell carcinoma is a highly lethal gynecologic cancer that depends heavily on mitochondrial respiration. Our biochemical and proteomic analyses reveal that ARID1A knockout cells exhibit marked upregulation of specific subunits within mitochondrial electron transport chain (ETC) Complexes I, III, and IV. However, this upregulation does not directly translate into increased sensitivity to broad-spectrum inhibitors targeting these complexes. These findings suggest that  ...[more]

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