PKD3 localizes to late endosomes to maintain Rab7-dependent endolysosomal homeostasis.

Elena Gutiérrez-Galindo, Katharina Jursik, Yannick Frey, Florian Meyer, Angelika Hausser

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In one paragraph

Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it

0cells of the map it votes in

0citing papers in PubMed

–field-weighted citation impact

1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

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0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Elena Gutiérrez-GalindoInstitute of Cell Biology and Immunology, University of Stuttgart, Allmandring 31, 70569 Stuttgart, Germany.

Katharina JursikInstitute of Cell Biology and Immunology, University of Stuttgart, Allmandring 31, 70569 Stuttgart, Germany.

Yannick FreyInstitute of Pathophysiology, Medical University of Innsbruck, Innrain 80/82, 6020 Innsbruck, Austria.

Florian MeyerInstitute of Cell Biology and Immunology, University of Stuttgart, Allmandring 31, 70569 Stuttgart, Germany.

Angelika HausserInstitute of Cell Biology and Immunology, University of Stuttgart, Allmandring 31, 70569 Stuttgart, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Protein kinase D3 (PKD3) is an important regulator of triple-negative breast cancer (TNBC) progression by promoting invasion, proliferation, and stem cell maintenance. However, the mechanism underlying these cellular functions has remained unclear. Here, we report that endogenous PKD3 localizes to Rab7-positive vesicles in MDA-MB-231 cells cultured on stiff matrices. Notably, PKD3 depletion results in smaller Rab7-positive vesicles with reduced retromer complex recruitment, leading to enhanced cathepsin D secretion. This correlates with impaired endosomal acidification, which is associated with dysregulated Wnt signaling and a decline in stemness. Our data thus unveil a previously unrecognized role of PKD3 in regulating endolysosomal dynamics that contributes to the maintenance of the cancer stem cell population in TNBC.

Indexed as

Biological sciencesDevelopmental biologyMolecular biology

Identifiers

PMID40970203

DOI10.1016/j.isci.2025.113408

PMCPMC12441718

What Socratic holds

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.