Evidence map›Paper›PMID 40719699›Full record

ArticleThe Journal of cell biology2025

STIM-IP3R crosstalk regulates migration of breast cancer cells.

Ruslana Militsin, Hadas Achildiev Cohen, Maya Hershfinkel, Ofek Levi, Stavit Drori, Adi Yifat Raz, Yuval Shaked, Raz Palty

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of cell biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

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

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Review
  2. Article
4 · The record

Corrections and comments

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

8 authors.

Ruslana MilitsinDepartment of Biochemistry, Technion Integrated Cancer Center, Ruth and Bruce Rappaport Faculty of Medicine, Technion - Israel Institute of Technology, Haifa, Israel.ORCID 0009-0000-0000-830X
Hadas Achildiev CohenDepartment of Biochemistry, Technion Integrated Cancer Center, Ruth and Bruce Rappaport Faculty of Medicine, Technion - Israel Institute of Technology, Haifa, Israel.ORCID 0009-0003-4858-5247
Maya HershfinkelDepartment of Biochemistry, Technion Integrated Cancer Center, Ruth and Bruce Rappaport Faculty of Medicine, Technion - Israel Institute of Technology, Haifa, Israel.ORCID 0009-0009-0769-3675
Ofek LeviDepartment of Biochemistry, Technion Integrated Cancer Center, Ruth and Bruce Rappaport Faculty of Medicine, Technion - Israel Institute of Technology, Haifa, Israel.ORCID 0009-0006-5521-2571
Stavit DroriDepartment of Biochemistry, Technion Integrated Cancer Center, Ruth and Bruce Rappaport Faculty of Medicine, Technion - Israel Institute of Technology, Haifa, Israel.ORCID 0009-0009-0037-8656
Adi Yifat RazDepartment of Biochemistry, Technion Integrated Cancer Center, Ruth and Bruce Rappaport Faculty of Medicine, Technion - Israel Institute of Technology, Haifa, Israel.ORCID 0009-0008-4393-001X
Yuval ShakedDepartment of Cell Biology and Cancer Science, Technion Integrated Cancer Center, Ruth and Bruce Rappaport Faculty of Medicine, Technion Israel Institute of Technology, Haifa, Israel.ORCID 0000-0001-9037-3895
Raz PaltyDepartment of Biochemistry, Technion Integrated Cancer Center, Ruth and Bruce Rappaport Faculty of Medicine, Technion - Israel Institute of Technology, Haifa, Israel.ORCID 0000-0001-6238-2399

Funding

Israeli Science Foundation 2123/22Rappaport InstituteTechnion-Israel Institute of Technology
6 · The paper itself

Abstract

Calcium ions (Ca2+) are crucial second messengers involved in numerous processes including tumorigenesis and cancer cell migration. Previous studies have shown that the endoplasmic reticulum (ER) Ca2+ sensors, stromal interaction molecules STIM1 and STIM2, are key regulators of cancer cell migration. In this study, using breast cancer cells lacking one or both STIM isoforms we show that although STIM proteins are critical regulators of cell migration, they are dispensable for this cellular activity. The mechanism underlying this complex effect involves functional crosstalk between STIM proteins and inositol 1,4,5-trisphosphate receptors (IP3Rs). Our findings indicate that beyond their classical role in store-operated Ca2+ entry, STIM proteins shape the spatial dynamics of IP3R-mediated Ca2+ release. Our results suggest that following ER Ca2+ depletion, the activated STIM proteins shift the pattern of IP3R-mediated Ca2+ release from a localized signal, which promotes cell migration, to a more diffuse signal, which attenuates cell migration.

Indexed as

Breast NeoplasmsCell MovementInositol 1,4,5-Trisphosphate ReceptorsNeoplasm ProteinsStromal Interaction Molecule 1Stromal Interaction Molecule 2CalciumCalcium SignalingCell Line, TumorEndoplasmic ReticulumFemaleHumansCalciumInositol 1,4,5-Trisphosphate ReceptorsNeoplasm ProteinsSTIM1 protein, humanSTIM2 protein, humanStromal Interaction Molecule 1Stromal Interaction Molecule 2

Identifiers

PMID40719699
PMCPMC12302952

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.