Evidence map›Paper›PMID 32545340›Full record

ReviewCancers2020

Active RAC1 Promotes Tumorigenic Phenotypes and Therapy Resistance in Solid Tumors.

Pradip De, Brett James Rozeboom, Jennifer Carlson Aske, Nandini Dey

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.3field-weighted citation impact, top 17% 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

21 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
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  6. RAC1 signaling in prostate cancer: VAV GEFs take center stage.Frontiers in cell and developmental biology · 2025
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  7. Review
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  19. The emerging role of the KCTD proteins in cancer.Cell communication and signaling : CCS · 2021
    Review
  20. 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

4 authors at 2 institutions in 1 country.

Pradip DeTranslational Oncology Laboratory, Avera Cancer Institute, Sioux Falls, SD 57105, USA.
Brett James RozeboomMSIV, SSOM, University of South Dakota, Vermillion, SD 57069, USA.ORCID 0000-0001-6856-0707
Jennifer Carlson AskeTranslational Oncology Laboratory, Avera Cancer Institute, Sioux Falls, SD 57105, USA.ORCID 0000-0001-9405-5464
Nandini DeyTranslational Oncology Laboratory, Avera Cancer Institute, Sioux Falls, SD 57105, USA.
University of South Dakota · USAvera Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acting as molecular switches, all three members of the Guanosine triphosphate (GTP)-ase-family, Ras-related C3 botulinum toxin substrate (RAC), Rho, and Cdc42 contribute to various processes of oncogenic transformations in several solid tumors. We have reviewed the distribution of patterns regarding the frequency of Ras-related C3 botulinum toxin substrate 1 (RAC1)-alteration(s) and their modes of actions in various cancers. The RAC1 hyperactivation/copy-number gain is one of the frequently observed features in various solid tumors. We argued that RAC1 plays a critical role in the progression of tumors and the development of resistance to various therapeutic modalities applied in the clinic. With this perspective, here we interrogated multiple functions of RAC1 in solid tumors pertaining to the progression of tumors and the development of resistance with a special emphasis on different tumor cell phenotypes, including the inhibition of apoptosis and increase in the proliferation, epithelial-to-mesenchymal transition (EMT), stemness, pro-angiogenic, and metastatic phenotypes. Our review focuses on the role of RAC1 in adult solid-tumors and summarizes the contextual mechanisms of RAC1 involvement in the development of resistance to cancer therapies.

Indexed as

angiogenesisapoptosisCSCEMTinvasionmetastasisproliferationRAC1resistancesolid tumors

Identifiers

PMID32545340
PMCPMC7352592
OpenAlexW3035555881

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.