Evidence map›Paper›PMID 36769280›Full record

ArticleInternational journal of molecular sciences2023

Ubiquitin-Related Modifier 1 (URM-1) Modulates Cx43 in Breast Cancer Cell Lines.

Layal El-Hajjar, Jessica Saliba, Mario Karam, Abdullah Shaito, Hiba El Hajj, Marwan El-Sabban

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2023. 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
0.3field-weighted citation impact, top 38% 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

0 citing papers in PubMed, 2 citations in OpenAlex.

No citing paper in PubMed yet.

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

6 authors at 3 institutions in 2 countries.

Layal El-HajjarDepartment of Anatomy, Cell Biology and Physiological Sciences, Faculty of Medicine, American University of Beirut, Beirut P.O. Box 11-0236, Lebanon.
Jessica SalibaDepartment of Biology, Faculty of Sciences, Lebanese University, Beirut P.O. Box 90656, Lebanon.
Mario KaramDepartment of Anatomy, Cell Biology and Physiological Sciences, Faculty of Medicine, American University of Beirut, Beirut P.O. Box 11-0236, Lebanon.
Abdullah ShaitoBiomedical Research Center, Qatar University Doha, Doha P.O. Box 2713, Qatar.ORCID 0000-0003-3524-7962
Hiba El HajjDepartment of Experimental Pathology, Immunology and Microbiology, Faculty of Medicine, American University of Beirut, Beirut P.O. Box 11-0236, Lebanon.ORCID 0000-0002-1069-0477
Marwan El-SabbanDepartment of Anatomy, Cell Biology and Physiological Sciences, Faculty of Medicine, American University of Beirut, Beirut P.O. Box 11-0236, Lebanon.
American University of Beirut · LBLebanese University · LBQatar University · QA

Funding

Lebanese National Council for Scientific Research NAMedical Practice Plan NAUniversity Research Board at the Faculty of Medicine at the American University of Beirut NA
6 · The paper itself

Abstract

Gap-junction-forming connexins are exquisitely regulated by post-translational modifications (PTMs). In particular, the PTM of connexin 43 (Cx43), a tumor suppressor protein, regulates its turnover and activity. Here, we investigated the interaction of Cx43 with the ubiquitin-related modifier 1 (URM-1) protein and its impact on tumor progression in two breast cancer cell lines, highly metastatic triple-negative MDA-MB-231 and luminal breast cancer MCF-7 cell lines. To evaluate the subsequent modulation of Cx43 levels, URM-1 was downregulated in these cells. The transcriptional levels of epithelial-to-mesenchymal transition (EMT) markers and the metastatic phenotype were assessed. We demonstrated that Cx43 co-localizes and interacts with URM-1, and URMylated Cx43 was accentuated upon cellular stress. The significant upregulation of small ubiquitin-like modifier-1 (SUMO-1) was also observed. In cells with downregulated URM-1, Cx43 expression significantly decreased, and SUMOylation by SUMO-1 was affected. The concomitant expression of EMT markers increased, leading to increased proliferation, migration, and invasion potential. Inversely, the upregulation of URM-1 increased Cx43 expression and reversed EMT-induced processes, underpinning a role for this PTM in the observed phenotypes. This study proposes that the URMylation of Cx43 in breast cancer cells regulates its tumor suppression properties and contributes to breast cancer cell malignancy.

Indexed as

Breast NeoplasmsConnexin 43Cell Line, TumorCell MovementCell ProliferationConnexinsEpithelial-Mesenchymal TransitionFemaleGap JunctionsHumansMCF-7 CellsUbiquitinUbiquitinsConnexin 43ConnexinsUbiquitinUbiquitinsUrm1 protein, humanbreast cancerCx43epithelial-to-mesenchymal transitionpost-translational modificationURM-1

Identifiers

PMID36769280
PMCPMC9917400
OpenAlexW4319158515

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.