Evidence map›Paper›PMID 24565984›Full record

ArticleOral oncology2014

Down regulation of RhoC by microRNA-138 results in de-activation of FAK, Src and Erk1/2 signaling pathway in head and neck squamous cell carcinoma.

Mozaffarul Islam, Jharna Datta, James C Lang, Theodoros N Teknos

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

Article in Oral oncology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

31 citing papers in PubMed, 47 citations in OpenAlex.

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  7. Role of RhoC in cancer cell migration.Cancer cell international · 2021
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Mozaffarul IslamDepartment of Otolaryngology-Head and Neck Surgery, The Ohio State University, Wexner Medical Center, Columbus, OH, USA; Arthur G. James Cancer Hospital and Richard J. Solove Research Institute, The Ohio State University, Wexner Medical Center, Columbus, OH, USA. Electronic address: Mozaffarul.Islam@osumc.edu.
Jharna DattaArthur G. James Cancer Hospital and Richard J. Solove Research Institute, The Ohio State University, Wexner Medical Center, Columbus, OH, USA.
James C LangDepartment of Otolaryngology-Head and Neck Surgery, The Ohio State University, Wexner Medical Center, Columbus, OH, USA; Arthur G. James Cancer Hospital and Richard J. Solove Research Institute, The Ohio State University, Wexner Medical Center, Columbus, OH, USA.
Theodoros N TeknosDepartment of Otolaryngology-Head and Neck Surgery, The Ohio State University, Wexner Medical Center, Columbus, OH, USA; Arthur G. James Cancer Hospital and Richard J. Solove Research Institute, The Ohio State University, Wexner Medical Center, Columbus, OH, USA.
The Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute · USThe Ohio State University Wexner Medical Center · US

Funding

Translational Therapeutics Research Program (TT)P30CA016058 · NCI · OHIO STATE UNIVERSITY · PI Tasleem J Padamsee · 1985 to 2026
$132.3M
NCI NIH HHS P30 CA016058
6 · The paper itself

Abstract

objectiveRhoC a pro-metastatic oncogene is constitutively active in many head and neck squamous cell carcinomas. MicroRNA-138 which possesses a documented tumor suppressor function can bind to the 3'UTR of RhoC mRNA and inhibit its activity. We hypothesize that miR-138 can inhibit the function of RhoC and consequently the activation of downstream target molecules involve in the signaling cascade. For this reason we investigated the role of miR-138 in HNSCC.

methodsIn vitro studies were carried out to evaluate the role of miR-138 in HNSCC cell lines and in primary tumors obtained from HNSCC patients. Real time RT-PCR, Western blot, cell motility, invasion and colony formation assays were performed according to standard procedures.

resultsData obtained by G-LISA and real time PCR shows an inverse correlation between RhoC expression and miR-138 in HNSCC cell lines. Additionally, we obtained a similar pattern of RhoC and miR-138 expression in primary tumors from HNSCC patients. Over expression of miR-138 in HNSCC lines showed down regulation of RhoC, as well as a decrease in cell motility, invasion colony and stress fiber formation. Furthermore, a significant down regulation was observed for FAK, Src and Erk(1/2) upon miR-138 overexpression.

conclusionThese findings strongly suggest that the inhibition of RhoC can be achieved by over expressing miR-138, which further attenuates the downstream signaling cascade leading to cancer progression and survival. Moreover, this study for the first time shows that down regulation of FAK, Src and Erk(1/2) by miR-138 overexpression is due to inhibition of RhoC in HNSCC.

Indexed as

Down-RegulationSignal Transduction3' Untranslated RegionsCarcinoma, Squamous CellCell Line, TumorFocal Adhesion Protein-Tyrosine KinasesHead and Neck NeoplasmsHumansMAP Kinase Signaling SystemMicroRNAsProto-Oncogene Proteins pp60(c-src)rhoC GTP-Binding Proteinrho GTP-Binding Proteins3' Untranslated RegionsFocal Adhesion Protein-Tyrosine KinasesMicroRNAsMIRN138 microRNA, humanProto-Oncogene Proteins pp60(c-src)rhoC GTP-Binding ProteinRHOC protein, humanrho GTP-Binding ProteinsErk(1/2)FAKHead and neck cancermiR-138RhoCSrc

Identifiers

PMID24565984
PMCPMC4296979
OpenAlexW1996044457

What OpenQuestion holds

Textmetadata
LicenceTDM
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.