Evidence map›Paper›PMID 37442828›Full record

ArticleCellular and molecular life sciences : CMLS2023

Sorcin promotes migration in cancer and regulates the EGF-dependent EGFR signaling pathways.

Claudia Tito, Ilaria Genovese, Flavia Giamogante, Anna Benedetti, Selenia Miglietta, Lucia Barazzuol, Loredana Cristiano, Alessia Iaiza, Sabatino Carolini, Luciana De Angelis and 12 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 7% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.

  1. Pooled it
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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

22 authors at 7 institutions in 2 countries.

Claudia TitoSection of Histology and Medical Embryology, Department of Anatomical, Histological, Forensic & Orthopaedic Sciences, Sapienza University of Rome, Via A. Scarpa, 14-16, 00161, Rome, Italy.
Ilaria GenoveseInstitute of Molecular Biology and Pathology, Italian National Research Council, IBPM-CNR, P.le A. Moro 5, 00185, Rome, Italy.
Flavia GiamoganteDepartment of Biomedical Sciences, University of Padova, Padua, Italy.
Anna BenedettiSection of Histology and Medical Embryology, Department of Anatomical, Histological, Forensic & Orthopaedic Sciences, Sapienza University of Rome, Via A. Scarpa, 14-16, 00161, Rome, Italy.
Selenia MigliettaSection of Human Anatomy, Department of Anatomical, Histological, Forensic & Orthopaedic Sciences, Sapienza University of Rome, Rome, Italy.
Lucia BarazzuolDepartment of Biomedical Sciences, University of Padova, Padua, Italy.
Loredana CristianoDepartment of Life, Health and Environmental Sciences, University of L'Aquila, L'Aquila, Italy.
Alessia IaizaSection of Histology and Medical Embryology, Department of Anatomical, Histological, Forensic & Orthopaedic Sciences, Sapienza University of Rome, Via A. Scarpa, 14-16, 00161, Rome, Italy.
Sabatino CaroliniInstitute of Molecular Biology and Pathology, Italian National Research Council, IBPM-CNR, P.le A. Moro 5, 00185, Rome, Italy.
Luciana De AngelisSection of Histology and Medical Embryology, Department of Anatomical, Histological, Forensic & Orthopaedic Sciences, Sapienza University of Rome, Via A. Scarpa, 14-16, 00161, Rome, Italy.
Silvia MasciarelliSection of Histology and Medical Embryology, Department of Anatomical, Histological, Forensic & Orthopaedic Sciences, Sapienza University of Rome, Via A. Scarpa, 14-16, 00161, Rome, Italy.
Stefania Annarita NottolaSection of Human Anatomy, Department of Anatomical, Histological, Forensic & Orthopaedic Sciences, Sapienza University of Rome, Rome, Italy.
Giuseppe FamiliariSection of Human Anatomy, Department of Anatomical, Histological, Forensic & Orthopaedic Sciences, Sapienza University of Rome, Rome, Italy.
Vincenzo PetrozzaDepartment of Medico-Surgical Sciences and Biotechnologies, Sapienza University of Rome, Latina, Italy.
Mattia LauriolaDepartment of Experimental, Diagnostic and Specialty Medicine (DIMES), University of Bologna, Bologna, Italy.
Luca TamagnoneDepartment of Life Science and Public Health, Histology and Embryology Unit - Catholic University of the Sacred Hearth, Fondazione Policlinico Gemelli - IRCCS, Rome, Italy.
Andrea IlariInstitute of Molecular Biology and Pathology, Italian National Research Council, IBPM-CNR, P.le A. Moro 5, 00185, Rome, Italy.
Tito CalìDepartment of Biomedical Sciences, University of Padova, Padua, Italy.
Hector H ValdiviaDepartment of Medicine, Cardiovascular Research Center, University of Wisconsin, Madison, WI, USA.
Carmen R ValdiviaDepartment of Medicine, Cardiovascular Research Center, University of Wisconsin, Madison, WI, USA.
Gianni ColottiInstitute of Molecular Biology and Pathology, Italian National Research Council, IBPM-CNR, P.le A. Moro 5, 00185, Rome, Italy.
Francesco FaziSection of Histology and Medical Embryology, Department of Anatomical, Histological, Forensic & Orthopaedic Sciences, Sapienza University of Rome, Via A. Scarpa, 14-16, 00161, Rome, Italy. francesco.fazi@uniroma1.it.ORCID http://orcid.org/0000-0003-2910-7912
Sapienza University of Rome · ITInstitute of Molecular Biology and Pathology · ITUniversity of Padua · ITUniversity of Wisconsin–Madison · USUniversità Cattolica del Sacro Cuore · ITUniversity of Bologna · ITUniversity of L'Aquila · IT

Funding

Ryanodine Receptors, Calcium-dependent Arrhythmias & HCMR01HL055438 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI VALDIVIA, HECTOR H · 1996 to 2023
$8.0M
Partial and Controlled Depletion of SR Calcium by RyR Agonists Prevents Calcium-dependent ArrhythmiasR01HL167195 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI Francisco J Alvarado, Hector H Valdivia · 2023 to 2026
$2.4M
NHLBI NIH HHS R01 HL055438NHLBI NIH HHS R01 HL167195
6 · The paper itself

Abstract

The epidermal growth factor receptor (EGFR) is one of the main tumor drivers and is an important therapeutic target for many cancers. Calcium is important in EGFR signaling pathways. Sorcin is one of the most important calcium sensor proteins, overexpressed in many tumors, that promotes cell proliferation, migration, invasion, epithelial-to-mesenchymal transition, malignant progression and resistance to chemotherapeutic drugs. The present work elucidates a functional mechanism that links calcium homeostasis to EGFR signaling in cancer. Sorcin and EGFR expression are significantly correlated and associated with reduced overall survival in cancer patients. Mechanistically, Sorcin directly binds EGFR protein in a calcium-dependent fashion and regulates calcium (dys)homeostasis linked to EGF-dependent EGFR signaling. Moreover, Sorcin controls EGFR proteostasis and signaling and increases its phosphorylation, leading to increased EGF-dependent migration and invasion. Of note, silencing of Sorcin cooperates with EGFR inhibitors in the regulation of migration, highlighting calcium signaling pathway as an exploitable target to enhance the effectiveness of EGFR-targeting therapies.

Indexed as

Epidermal Growth FactorNeoplasmsCalciumCell Line, TumorCell MovementErbB ReceptorsHumansSignal TransductionCalciumEGFR protein, humanEpidermal Growth FactorErbB ReceptorsCalciumCancerEGFEGFREpithelial-to-mesenchymal transitionInvasionMigrationSignalingSorcin

Identifiers

PMID37442828
PMCPMC10345051
OpenAlexW4384155045

What OpenQuestion 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 OpenQuestion graph.