Evidence map›Paper›PMID 35722965›Full record

ArticleAutophagy2023

Tumor-derived CTF1 (cardiotrophin 1) is a critical mediator of stroma-assisted and autophagy-dependent breast cancer cell migration, invasion and metastasis.

Yunus Akkoc, Kubilay Dalci, Hacer Ezgi Karakas, Secil Erbil-Bilir, Orcun Yalav, Gurhan Sakman, Faruk Celik, Soykan Arikan, Umit Zeybek, Melek Ergin and 5 more

Open access · greenAbstract read
In one paragraph

Article in Autophagy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
5.8field-weighted citation impact, top 3% of its field
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

30 citing papers in PubMed, 41 citations in OpenAlex.

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  15. Exploiting Matrix Stiffness to Overcome Drug Resistance.ACS biomaterials science & engineering · 2024
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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

15 authors at 7 institutions in 2 countries.

Yunus AkkocKoç University Research Center for Translational Medicine (KUTTAM), Istanbul, Turkey.
Kubilay DalciFaculty of Medicine, Department of General Surgery, Çukurova University, Adana, Turkey.
Hacer Ezgi KarakasDepartment of Biotechnology, Sabanci University Nanotechnology Research and Application Center (SUNUM), Istanbul, Turkey.
Secil Erbil-BilirDepartment of Biotechnology, Sabanci University Nanotechnology Research and Application Center (SUNUM), Istanbul, Turkey.
Orcun YalavFaculty of Medicine, Department of General Surgery, Çukurova University, Adana, Turkey.
Gurhan SakmanFaculty of Medicine, Department of General Surgery, Çukurova University, Adana, Turkey.
Faruk CelikDepartment of Molecular Medicine, Istanbul University Aziz Sancar Institute of Experimental Medicine, Istanbul, Turkey.
Soykan ArikanDepartment of General Surgery, Ministry of Health Samatya Training and Research Hospital, Istanbul, Turkey.
Umit ZeybekDepartment of Molecular Medicine, Istanbul University Aziz Sancar Institute of Experimental Medicine, Istanbul, Turkey.
Melek ErginFaculty of Medicine, Department of Pathology, Çukurova University, Adana, Turkey.
Hikmet AkkizFaculty of Medicine, Department of Gastroenterology, Çukurova University, Adana, Turkey.
Ece DilegeKoç University Hospital, Department of General Surgery, Koç University Medical School, Istanbul, Turkey.
Joern DengjelDepartment of Biology, University of Fribourg, Fribourg, Switzerland.ORCID 0000-0002-9453-4614
A Isin Dogan-EkiciSchool of Medicine, Department of Pathology, Acibadem Mehmet Ali Aydınlar University, Istanbul, Turkey.
Devrim GozuacikKoç University Research Center for Translational Medicine (KUTTAM), Istanbul, Turkey.ORCID 0000-0001-7739-2346
Cukurova University · TRSabancı Üniversitesi · TRIstanbul University · TRKent Hastanesi · TRKoç University · TRMinistry of Health · TRUniversity of Fribourg · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macroautophagy/autophagy is an evolutionarily conserved cellular stress response mechanism. Autophagy induction in the tumor microenvironment (stroma) has been shown to support tumor metabolism. However, cancer cell-derived secreted factors that initiate communication with surrounding cells and stimulate autophagy in the tumor microenvironment are not fully documented. We identified CTF1/CT-1 (cardiotrophin 1) as an activator of autophagy in fibroblasts and breast cancer-derived carcinoma-associated fibroblasts (CAFs). We showed that CTF1 stimulated phosphorylation and nuclear translocation of STAT3, initiating transcriptional activation of key autophagy proteins. Additionally, following CTF1 treatment, AMPK and ULK1 activation was observed. We provided evidence that autophagy was important for CTF1-dependent ACTA2/α-SMA accumulation, stress fiber formation and fibroblast activation. Moreover, promotion of breast cancer cell migration and invasion by activated fibroblasts depended on CTF1 and autophagy. Analysis of the expression levels of CTF1 in patient-derived breast cancer samples led us to establish a correlation between CTF1 expression and autophagy in the tumor stroma. In line with our

Indexed as

AutophagyBreast NeoplasmsCytokinesAnimalsCell Line, TumorCell MovementFemaleFibroblastsHumansInterleukin-6MiceTransforming Growth Factor betacardiotrophin 1CytokinesInterleukin-6Transforming Growth Factor betaAutophagybreast cancercarcinoma-associated fibroblastcardiotrophin 1tumor stroma

Identifiers

PMID35722965
PMCPMC9809961
OpenAlexW4283119185

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.