Evidence map›Paper›PMID 36469134›Full record

ArticleCellular and molecular life sciences : CMLS2022

RhoC in association with TET2/WDR5 regulates cancer stem cells by epigenetically modifying the expression of pluripotency genes.

Pavana Thomas, Sweta Srivastava, Avinash H Udayashankara, Samyuktha Damodaran, Lokendra Yadav, Boby Mathew, Srinag Bangalore Suresh, Amit Kumar Mandal, Nirmala Srikantia

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

Article in Cellular and molecular life sciences : CMLS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.4field-weighted citation impact, top 40% 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

2 citing papers in PubMed, 5 citations in OpenAlex.

  1. Review
  2. Review
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

9 authors at 2 institutions in 1 country.

Pavana ThomasTranslational and Molecular Biology Laboratory (TMBL), Division of Molecular Biology and Genetics, St. John's Research Institute (SJRI), St. John's Medical College, Bangalore, 560034, India.
Sweta SrivastavaTranslational and Molecular Biology Laboratory (TMBL), Division of Molecular Biology and Genetics, St. John's Medical College Hospital, Bangalore, 560034, India. sweta.s@stjohns.in.ORCID http://orcid.org/0000-0001-6063-0811
Avinash H UdayashankaraDepartment of Radiation Oncology, St John's Medical College Hospital, Bangalore, 560034, India.
Samyuktha DamodaranTranslational and Molecular Biology Laboratory (TMBL), Division of Molecular Biology and Genetics, St. John's Research Institute (SJRI), St. John's Medical College, Bangalore, 560034, India.
Lokendra YadavTranslational and Molecular Biology Laboratory (TMBL), Division of Molecular Biology and Genetics, St. John's Medical College Hospital, Bangalore, 560034, India.
Boby MathewClinical Proteomics Unit, Division of Molecular Medicine, St. John's Research Institute (SJRI), St. John's Medical College, Bangalore, 560034, India.
Srinag Bangalore SureshTranslational and Molecular Biology Laboratory (TMBL), Division of Molecular Biology and Genetics, St. John's Research Institute (SJRI), St. John's Medical College, Bangalore, 560034, India.
Amit Kumar MandalClinical Proteomics Unit, Division of Molecular Medicine, St. John's Research Institute (SJRI), St. John's Medical College, Bangalore, 560034, India.
Nirmala SrikantiaDepartment of Radiation Oncology, St John's Medical College Hospital, Bangalore, 560034, India.
St.John's Medical College Hospital · INUniversity of Trans-Disciplinary Health Sciences and Technology · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Emerging evidence illustrates that RhoC has divergent roles in cervical cancer progression where it controls epithelial to mesenchymal transition (EMT), migration, angiogenesis, invasion, tumor growth, and radiation response. Cancer stem cells (CSCs) are the primary cause of recurrence and metastasis and exhibit all of the above phenotypes. It, therefore, becomes imperative to understand if RhoC regulates CSCs in cervical cancer. In this study, cell lines and clinical specimen-based findings demonstrate that RhoC regulates tumor phenotypes such as clonogenicity and anoikis resistance. Accordingly, inhibition of RhoC abrogated these phenotypes. RNA-seq analysis revealed that RhoC over-expression resulted in up-regulation of 27% of the transcriptome. Further, the Infinium MethylationEPIC array showed that RhoC over-expressing cells had a demethylated genome. Studies divulged that RhoC via TET2 signaling regulated the demethylation of the genome. Further investigations comprising ChIP-seq, reporter assays, and mass spectrometry revealed that RhoC associates with WDR5 in the nucleus and regulates the expression of pluripotency genes such as Nanog. Interestingly, clinical specimen-based investigations revealed the existence of a subset of tumor cells marked by RhoC

Indexed as

DioxygenasesUterine Cervical NeoplasmsCell Line, TumorCell MovementCell ProliferationDNA-Binding ProteinsEpigenesis, GeneticEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansIntracellular Signaling Peptides and ProteinsNeoplastic Stem CellsrhoC GTP-Binding ProteinDioxygenasesDNA-Binding ProteinsIntracellular Signaling Peptides and ProteinsrhoC GTP-Binding ProteinRHOC protein, humanTET2 protein, humanWDR5 protein, humanChIP-seqInfinium MethylationEPIC arrayMolecular drug targetsRadiosensitizationSelf-renewal

Identifiers

PMID36469134
PMCPMC11073244
OpenAlexW4310785202

What OpenQuestion holds

Textmetadata
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.