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Breast cancer cell lines in co-culture with hESC-derived nerual progenitor cells

ABSTRACT: In this study breast cancer cell lines were co-cultured with hESC-derived neural progenitor cells. Our aim was to determine how the breast cancer cellular proteomes were changed after one week in co-culture.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Epithelial Cell, Cell Culture, Neural Progenitor Cell

DISEASE(S): Breast Cancer

SUBMITTER: Heidrun Vethe

LAB HEAD: Lars A. Akslen

PROVIDER: PXD040662 | Pride | 2025-05-06

REPOSITORIES: Pride

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			Action	DRS
	560076_a27239_hv_hum16.mzIdentML	Mzid
	560077_a27238_hv_hum16.mzIdentML	Mzid
	560078_a27237_hv_hum16.mzIdentML	Mzid
	560079_a27236_hv_hum16.mzIdentML	Mzid
	560080_a27241_hv_hum16.mzIdentML	Mzid

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Publications

Global and single-cell proteomics view of the co-evolution between neural progenitors and breast cancer cells in a co-culture model.

Bjørnstad Ole Vidhammer OV Carrasco Manuel M Finne Kenneth K Ardawatia Vandana V Winge Ingeborg I Askeland Cecilie C Arnes Jarle B JB Knutsvik Gøril G Kleftogiannis Dimitrios D Paulo Joao A JA Akslen Lars A LA Vethe Heidrun H

EBioMedicine 20240904

<h4>Background</h4>Presence of nerves in tumours, by axonogenesis and neurogenesis, is gaining increased attention for its impact on cancer initiation and development, and the new field of cancer neuroscience is emerging. A recent study in prostate cancer suggested that the tumour microenvironment may influence cancer progression by recruitment of Doublecortin (DCX)-expressing neural progenitor cells (NPCs). However, the presence of such cells in human breast tumours has not been comprehensively ...[more]

PMID: 39232464

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Breast cancer cell lines in co-culture with hESC-derived nerual progenitor cells

Project description:In this study breast cancer cell lines were co-cultured with hESC-derived neural progenitor cells. Our aim was to determine how the breast cancer cellular proteomes were changed after one week in co-culture.

2025-05-06 | PXD044553 | Pride

MCL-1 Drives a Metabolic Dependency on Fatty Acid Oxidation in Cancer Independent of its Anti-Apoptotic Function

Project description:MCL-1 is an anti-apoptotic BCL-2 family protein essential to the survival of diverse cell types and is a major driver of cancer and chemoresistance. The unique oncogenic supremacy of MCL-1, as compared to its anti-apoptotic homologs, suggests that it has additional functions to complement apoptotic suppression. Here, we find that MCL-1-dependent hematologic cancer cells selectively rely on fatty acid oxidation (FAO) as a fuel source due to metabolic wiring enforced by MCL-1 itself. Importantly, this metabolic function is independent of anti-apoptotic activity, as demonstrated by metabolomic, proteomic, and genomic profiling of MCL-1-dependent leukemia cells lacking pro-apoptotic BAX and BAK. Genetic deletion of Mcl-1 results in selective downregulation of proteins within the FAO pathway, accompanied by cell death upon glucose deprivation despite apoptotic blockade. Our data reveal that MCL-1 drives a programmatic dependency on FAO in hematologic cancer cells, which can be effectively targeted by FAO inhibitors.

2022-10-03 | PXD031364 | Pride

HEK293T cell degradome (pulse chase) analysis upon 12h Torin1 treatment. Related to Supplementary Table 3 from An et al (2020)

Project description:HEK293T Azidohomoalanine (AHA) Pulse Chase (degradome) experiment, were cells from various genetic background (WT, ATG7-/-, RB1CC1-/-) are treated or not with Torin1 for 12h. Samples are Biotin-click, and streptavidin enriched.

2020-04-30 | PXD017857 | Pride

HEK293T cell proteome abundance (WT vs NUFIP1 knock-out). Related to Supplementary Table 5 from An et al (2020)

Project description:HEK293T cells proteome comparison with or without NUFIP1 deletion. TMT channels 128n, 128c, 130c, 131n and 131c were not used for this analysis.

2020-04-30 | PXD017858 | Pride

HEK293 cell proteome remodeling upon Torin1 treatment or amino acid withdraw. Related to Supplementary Table 1 from An et al (2020)

Project description:HEK293 cells with two genotype (WT or ATCG5 KO), treated with Torin1 or amino acid withdraw. TMT 11 plex.

2020-07-12 | PXD017852 | Pride

HEK293T cell proteome remodeling upon 6-MP treatment. Related to Supplementary Table 6 from An et al (2020)

Project description:Total proteome abundance measurement after 24h 6-MP treatment in WT or ATG5 KO HEK293T cells. Channels 128n, 128c, 129n, 129c are not used for this analysis.

2020-04-30 | PXD017859 | Pride

Pleiotropic tumor suppressive functions of PTEN missense mutations during gliomagenesis

Project description:PTEN plays a crucial role in preventing the development of glioblastoma (GBM), a severe and untreatable brain cancer. In GBM, most PTEN deficiencies arise from missense mutations, many of which have not been thoroughly examined. Here, we leveraged genetically modified mice and matched isogenic astrocyte cell cultures to investigate how specific and clinically relevant PTEN mutations (G36E, L42R, C105F, and R173H) behave in the development of GBM driven by EGFR. We report that the tumor-suppressive abilities of these PTEN mutants do not depend on their ability to act as lipid phosphatases but are instead related to their increased presence at the cell membrane. Moreover, these PTEN mutations led to heightened EGFR activity by keeping EGFR within endomembranes longer, affecting its signaling behavior. Through comprehensive studies on global protein phosphorylation and kinase library analyses in cells with the G36E and L42R PTEN mutations, we identified distinct cancer-promoting pathways activated by EGFR, offering new targets for treating GBM with these PTEN alterations.

2025-05-06 | PXD051485 | Pride

HEK293T cell translatome analysis upon Torin1 treatment or single amino acid withdrawal. Related to Supplementary Table 2 from An et al (2020)

Project description:HEK293T subject to Torin1 treatment or amino acid withdraw dataset and translatome analysis was determined using Azidohomoalanine (AHA) incorportation, Biotin-click, and streptavidin enrichment. TMT 10plex labelling was used. Three genotypes, WT (24 fractions), ATG7 KO (HA-9-53-1 single shot), RB1CC1 KO (HA-9-53-2 single shot).

2020-04-30 | PXD018252 | Pride

HEK293T cell degradome (pulse chase) time course (5h, 10, 15h) analysis upon Torin1 treatment. Related to Supplementary Table 3 from An et al (2020)

Project description:HEK293T Azidohomoalanine (AHA) Pulse Chase (degradome) time course experiment, were cells from various genetic background (WT, ATG7-/-, RB1CC1-/-) are treated or not with Torin1 for 5h, 10h or 15h. Samples are Biotin-click, and streptavidin enriched, digested and labeled with TMTpro 16plex.

2020-04-30 | PXD018158 | Pride

Matrisome Proteomics Reveals Novel Mediators of Muscle Remodeling with Aerobic Exercise Training

Project description:Skeletal muscle has a unique ability to remodel in response to stimuli such as contraction and aerobic exercise training. Phenotypic changes in muscle that occur with training such as a switch to a more oxidative fiber type, and increased capillary density contribute to the well-known health benefits of aerobic exercise. The muscle matrisome likely plays an important role in muscle remodeling with exercise. However, due to technical limitations in studying muscle ECM proteins, which are highly insoluble, little is known about the muscle matrisome and how it contributes to muscle remodeling. Here, we utilized two-fraction methodology to extract muscle proteins, combined with multiplexed tandem mass tag proteomic technology to identify 161 unique ECM proteins in mouse skeletal muscle. In addition, we demonstrate that aerobic exercise training induces remodeling of a significant proportion of the muscle matrisome. We performed follow-up experiments to validate exercise-regulated ECM targets in a separate cohort of mice using Western blotting and immunofluorescence imaging. Our data demonstrate that changes in several key ECM targets are strongly associated with muscle remodeling processes such as increased capillary density in mice. We also identify LOXL1 as a novel muscle ECM target associated with aerobic capacity in humans. In addition, publically available data and databases were used for in silico modeling to determine the likely cellular sources of exercise-induced ECM remodeling targets and identify ECM interaction networks. This work greatly enhances our understanding of ECM content and function in skeletal muscle and demonstrates an important role for ECM remodeling in the adaptive response to exercise.

2024-07-30 | PXD053003 | Pride

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