Evidence map›Paper›PMID 38733529›Full record

ReviewCellular and molecular life sciences : CMLS2024

Circular RNAs in EMT-driven metastasis regulation: modulation of cancer cell plasticity, tumorigenesis and therapy resistance.

Milad Ashrafizadeh, Jingyuan Dai, Pedram Torabian, Noushin Nabavi, Amir Reza Aref, Alaa A A Aljabali, Murtaza Tambuwala, Minglin Zhu

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
–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

42 citing papers in PubMed, 1 synthesis or guideline 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

8 authors.

Milad AshrafizadehDepartment of Radiation Oncology, Shandong Provincial Key Laboratory of Radiation Oncology, Shandong Cancer Hospital and Institute, Shandong First Medical University, Shandong Academy of Medical Sciences, Jinan, Shandong 250000, China.
Jingyuan DaiSchool of computer science and information systems, Northwest Missouri State University, Maryville, MO, 64468, USA. S571358@nwmissouri.edu.
Pedram TorabianCumming School of Medicine, Arnie Charbonneau Cancer Research Institute, University of Calgary, Calgary, AB, T2N 4Z6, Canada.
Noushin NabaviDepartment of Urologic Sciences and Vancouver Prostate Centre, University of British Columbia, Vancouver, BC, V6H3Z6, Canada.
Amir Reza ArefBelfer Center for Applied Cancer Science, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.
Alaa A A AljabaliFaculty of Pharmacy, Department of Pharmaceutics and Pharmaceutical Technology, Yarmouk University, Irbid, Jordan.
Murtaza TambuwalaLincoln Medical School, University of Lincoln, Brayford Pool Campus, Lincoln, LN6 7TS, UK. mtambuwala@lincoln.ac.uk.ORCID http://orcid.org/0000-0001-8499-9891
Minglin ZhuDepartment of Cardiovascular Surgery, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, China. zhuminglin@whu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The non-coding RNAs comprise a large part of human genome lack of capacity in encoding functional proteins. Among various members of non-coding RNAs, the circular RNAs (circRNAs) have been of importance in the pathogenesis of human diseases, especially cancer. The circRNAs have a unique closed loop structure and due to their stability, they are potential diagnostic and prognostic factors in cancer. The increasing evidences have highlighted the role of circRNAs in the modulation of proliferation and metastasis of cancer cells. On the other hand, metastasis has been responsible for up to 90% of cancer-related deaths in patients, requiring more investigation regarding the underlying mechanisms modulating this mechanism. EMT enhances metastasis and invasion of tumor cells, and can trigger resistance to therapy. The cells demonstrate dynamic changes during EMT including transformation from epithelial phenotype into mesenchymal phenotype and increase in N-cadherin and vimentin levels. The process of EMT is reversible and its reprogramming can disrupt the progression of tumor cells. The aim of current review is to understanding the interaction of circRNAs and EMT in human cancers and such interaction is beyond the regulation of cancer metastasis and can affect the response of tumor cells to chemotherapy and radiotherapy. The onco-suppressor circRNAs inhibit EMT, while the tumor-promoting circRNAs mediate EMT for acceleration of carcinogenesis. Moreover, the EMT-inducing transcription factors can be controlled by circRNAs in different human tumors.

Indexed as

CarcinogenesisDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionNeoplasm MetastasisNeoplasmsRNA, CircularAnimalsCell PlasticityGene Expression Regulation, NeoplasticHumansRNA, Circularcancer cell plasticitycancer malignancycircRNAsDrug resistanceEMTRNA transcripts

Identifiers

PMID38733529
PMCPMC11088560

What OpenQuestion holds

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LicenceCC BY
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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.