Evidence map›Paper›PMID 38822973›Full record

ReviewMolecular biology reports2024

The scaffold protein disabled 2 (DAB2) and its role in tumor development and progression.

Disha V Pandya, Rajsi V Parikh, Ruhanahmed M Gena, Nirjari R Kothari, Priyajeet S Parekh, Mehul R Chorawala, Maharsh A Jani, Mayur R Yadav, Palak A Shah

RetractedAbstract readReviewRetracted Publication
PubMed Publisher
In one paragraph

Review in Molecular biology reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. 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

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.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors.

Disha V Pandya *Department of Pharmacology and Pharmacy Practice, L. M. College of Pharmacy, Opp. Gujarat University, Ahmedabad, Gujarat, 380009, India.ORCID http://orcid.org/0000-0002-7832-9282
Rajsi V Parikh *Department of Pharmacology and Pharmacy Practice, L. M. College of Pharmacy, Opp. Gujarat University, Ahmedabad, Gujarat, 380009, India.ORCID http://orcid.org/0000-0003-0766-7337
Ruhanahmed M Gena *Department of Pharmacology and Pharmacy Practice, L. M. College of Pharmacy, Opp. Gujarat University, Ahmedabad, Gujarat, 380009, India.ORCID http://orcid.org/0000-0002-3211-5406
Nirjari R KothariDepartment of Pharmacology and Pharmacy Practice, L. M. College of Pharmacy, Opp. Gujarat University, Ahmedabad, Gujarat, 380009, India.ORCID http://orcid.org/0000-0001-5614-2081
Priyajeet S ParekhPharmacy Practice Division, AV Pharma LLC, 1545 University Blvd N Ste A, Jacksonville, FL, 32211, USA.ORCID http://orcid.org/0009-0002-6284-8771
Mehul R ChorawalaDepartment of Pharmacology and Pharmacy Practice, L. M. College of Pharmacy, Opp. Gujarat University, Ahmedabad, Gujarat, 380009, India. mchorawalaresearch@gmail.com.ORCID http://orcid.org/0000-0002-3724-0986
Maharsh A JaniPharmacy Practice Division, Anand Niketan, Shilaj, Ahmedabad, Gujarat, 380059, India.ORCID http://orcid.org/0009-0007-3847-1536
Mayur R YadavDepartment of Pharmacy Practice and Administration, Western University of Health Science, 309 E Second St, Pomona, CA, 91766, USA.ORCID http://orcid.org/0009-0001-7751-1357
Palak A ShahDepartment of Pharmacology and Pharmacy Practice, K. B. Institute of Pharmaceutical Education and Research, Gandhinagar, Gujarat, 382023, India.ORCID http://orcid.org/0000-0002-2546-0906

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDisabled 2 (DAB2) is a multifunctional protein that has emerged as a critical component in the regulation of tumor growth. Its dysregulation is implicated in various types of cancer, underscoring its importance in understanding the molecular mechanisms underlying tumor development and progression. This review aims to unravel the intricate molecular mechanisms by which DAB2 exerts its tumor-suppressive functions within cancer signaling pathways. METHODS AND

resultsWe conducted a comprehensive review of the literature focusing on the structure, expression, physiological functions, and tumor-suppressive roles of DAB2. We provide an overview of the structure, expression, and physiological functions of DAB2. Evidence supporting DAB2's role as a tumor suppressor is explored, highlighting its ability to inhibit cell proliferation, induce apoptosis, and modulate key signaling pathways involved in tumor suppression. The interaction between DAB2 and key oncogenes is examined, elucidating the interplay between DAB2 and oncogenic signaling pathways. We discuss the molecular mechanisms underlying DAB2-mediated tumor suppression, including its involvement in DNA damage response and repair, regulation of cell cycle progression and senescence, and modulation of epithelial-mesenchymal transition (EMT). The review explores the regulatory networks involving DAB2, covering post-translational modifications, interactions with other tumor suppressors, and integration within complex signaling networks. We also highlight the prognostic significance of DAB2 and its role in pre-clinical studies of tumor suppression.

conclusionThis review provides a comprehensive understanding of the molecular mechanisms by which DAB2 exerts its tumor-suppressive functions. It emphasizes the significance of DAB2 in cancer signaling pathways and its potential as a target for future therapeutic interventions.

Indexed as

Adaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsNeoplasmsSignal TransductionAnimalsApoptosisCarcinogenesisCell ProliferationDisease ProgressionEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansTumor Suppressor ProteinsAdaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsDAB2 protein, humanTumor Suppressor ProteinsApoptosisCell proliferationDisabled 2 (DAB2)DNA damage responseEpithelial-mesenchymal transition (EMT)Oncogenic signallingTumor microenvironment (TME)Tumor suppressionWnt signaling

Identifiers

PMID38822973

What OpenQuestion holds

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Registered trials

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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 OpenQuestion graph.