Michalis Gounis

Uridine phosphorylase-1 supports metastasis by altering immune and extracellular matrix landscapes | EMBO reports imageimageMetastatic primary tumours upregulate Upp1 in neutrophils, which elevates circulating uracil. UPP1-expressing neutrophils accumulate in the lung where they inhibit CD8+ T cells, promote fibr...

Delighted to share that our work “Uridine Phosphorylase-1 supports metastasis by altering immune and extracellular matrix landscapes” was published today in @emboreports.org, describing how neutrophil metabolism influences niche priming to support metastasis (1/14) www.embopress.org/doi/full/10....

Figure showing the building MatriComDB, an omnibus database of matrisome protein interactions.

Rijuta Lamba, Alexandra Naba @nabalabuic.bsky.social, @valerioizzi.bsky.social and team present MatriCom, a single-cell RNA-sequencing data mining tool to infer cell–ECM interactions.
Highlight: journals.biologists.com/jcs/article/...
Article: journals.biologists.com/jcs/article/...
#OpenAccess

Differential roles of cyclin–CDK1 complexes in cell migration and invasion Highlighted Article: Cyclin–CDK1 complexes have a previously undiscovered role in regulating normal and cancer cell migration in 3D matrices.

Pleased that our latest paper is now out in @jcellsci.bsky.social, in collaboration with @drmcjones.bsky.social and others from Manchester and Plymouth: Differential roles of cyclin–CDK1 complexes in cell migration and invasion url: journals.biologists.com/jcs/article/...

EPLINα controls integrin recycling from Rab21 endosomes to drive breast cancer cell migration Epithelial protein lost in neoplasm (EPLIN), an actin-binding protein, has been described as both a tumor promoter and tumor suppressor in different c…

Latest from Ivaska Lab ▶️ Niklas Jäntti et al delve deep into the roles of EPLINα/β on integrin trafficking and breast cancer outcomes!

Congratulations to all the authors!

Check the paper out here: www.sciencedirect.com/science/arti...

EPLINα controls integrin recycling from Rab21 endosomes to drive breast cancer cell migration Epithelial protein lost in neoplasm (EPLIN), an actin-binding protein, has been described as both a tumor promoter and tumor suppressor in different c…

Excited to share our most recent study on #integrintraffic #cancer #migration #focaladhesion by @ivaskalab.bsky.social @drpaulinamoreno.bsky.social Niklas Jäntti et al www.sciencedirect.com/science/arti...

Great opportunity for a Research Support Officer to join @cellbiol-mrclmb.bsky.social, supporting @deriverylab.bsky.social in their studies of the molecular mechanisms behind receptor sorting in endosomes.
More info: www.nature.com/naturecareer...
Apply by 10 JUL
#ScienceJobs

Are you looking for a postdoc?
I will be looking for 2-4 people after the summer to join the lab !!
Do not hesitate to reach out and disseminate !!

Dynamic regulation of integrin β1 phosphorylation supports invasion of breast cancer cells - Nature Cell Biology Conway et al. show that integrin β1 phosphorylation is regulated through balanced activities of tyrosine kinases, such as Src and Arg, and phosphatases, such as PTP-PEST and Shp2, facilitating invadop...

☕Conway et al. show that #integrin β1 phosphorylation is regulated through balanced activities of tyrosine kinases, such as Src and Arg, and phosphatases, such as PTP-PEST and Shp2, facilitating invadopodia formation and invasion of #BreastCancer cells.
bit.ly/4n4v3JS

Congratulations @louisefets.bsky.social and team, beautiful work!! 👏👏
www.biorxiv.org/content/10.1...

Thank you so much Kirsteen 😊

Vassili, thank you very much for your kind words 😊

Martha, thank you for your support and kind words 😊

@cassiejclarke.bsky.social, thank you very much for the wonderful supervision 😊

Thank you very much Paulina 😄

Thank you very much Guillaume 😊

a cartoon dog is reading a book in a bed ALT: a cartoon dog is reading a book in a bed

10/ Massive thanks to @cassiejclarke.bsky.social and Jim for the wonderful supervision and @cancerresearchuk.org for the funding.
@uofglasgow.bsky.social @uofgcancersciences.bsky.social

Hope you enjoy reading!!

9/ Grateful to everyone that made this possible, especially members of the Norman lab for their great contribution @vanecitav.bsky.social @ruhi-d.bsky.social and members of the @ivaskalab.bsky.social for the unwavering support.

8/ Profoundly thankful to D. Sumpton, E. Shokry, S.Tardito for their metabolic expertise, K. Blyth and @louisemitchell21.bsky.social for their invaluable insights into the in vivo models. All the core facilities and services @cruk-si.bsky.social for the amazing work.

7/ Interestingly, disruption of Rab27s opposes EV release from primary tumour cells, but not from micrometastatic cells. Lastly, we show that the switch to nSM2-dependent EV release enables micrometastatic cells to influence #ECM deposition by fibroblasts to foster an invasive #microenvironment.

6/ Following the observation that ceramides are enriched in micrometastatic cells, we disrupted the expression of n. sphingomyelinases known to influence EV release. We found that reduction of nSM2, but not nSM1, significantly reduces ceramide levels and EV release from micrometastatic cells.

5/ In addition to their altered polar metabolism, we uncover that micrometastatic cells display elevated levels of distinct #ceramide species, which are also enriched in their EVs and are present at significantly higher levels in the plasma of metastatic breast cancer patients.

4/ Given the importance of #EVs in metastatic niche priming, we sought to examine the relationship of EV release from micrometastatic cells to their altered metabolism. We found that decreased ability to synthesise glutathione is associated with increased EV release.

3/We further demonstrate that proline and glutathione pathways compete for glutamine-derived carbons in micrometastatic cells. The adoption of this metabolic profile, in which proline and glutathione levels are, respectively, elevated and suppressed, is a feature unique to micrometastatic cells.

2/ We generated isogenic cells from primary mammary tumours and their corresponding lung micrometastases. We show that micrometastatic cells increase proline production and circulating proline is significantly elevated in mice and patients with metastatic disease.

a cartoon dog is reading a book in a bed ALT: a cartoon dog is reading a book in a bed

10/ Massive thanks to @cassiejclarke.bsky.social and Jim for the wonderful supervision and @cancerresearchuk.org for the funding.
@uofglasgow.bsky.social @uofgcancersciences.bsky.social

Hope you enjoy reading!!

9/ Grateful to everyone that made this possible, especially members of the Norman lab for their great contribution @vanecitav.bsky.social @ruhi-d.bsky.social and members of the @ivaskalab.bsky.social for the unwavering support.

8/ Profoundly thankful to D. Sumpton, E. Shokry, S.Tardito for their metabolic expertise, K. Blyth and @louisemitchell21.bsky.social for their invaluable insights into the in vivo models. All the core facilities and services @cruk-si.bsky.social for the amazing work.

7/ Interestingly, disruption of Rab27s opposes EV release from primary tumour cells, but not from micrometastatic cells. Lastly, we show that the switch to nSM2-dependent EV release enables micrometastatic cells to influence #ECM deposition by fibroblasts to foster an invasive #microenvironment.

6/ Following the observation that ceramides are enriched in micrometastatic cells, we disrupted the expression of n. sphingomyelinases known to influence EV release. We found that reduction of nSM2, but not nSM1, significantly reduces ceramide levels and EV release from micrometastatic cells.

5/ In addition to their altered polar metabolism, we uncover that micrometastatic cells display elevated levels of distinct #ceramide species, which are also enriched in their EVs and are present at significantly higher levels in the plasma of metastatic breast cancer patients.