Evidence map›Paper›PMID 27567435›Full record

ArticleOral surgery, oral medicine, oral pathology and oral radiology2016

Transforming growth factor-β1 activates ΔNp63/c-Myc to promote oral squamous cell carcinoma.

Lihua Hu, Jingpeng Liu, Zhi Li, Chunling Wang, Ali Nawshad

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

Article in Oral surgery, oral medicine, oral pathology and oral radiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

6 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 2 countries.

Lihua HuDepartment of Oral Biology, University of Nebraska Medical Center, Lincoln, NE, USA; Shandong Provincial Key Laboratory of Oral Biomedicine, Department of Orthodontics, School of Stomatology, Shandong University, Jinan, Shandong, P.R. China.
Jingpeng LiuDepartment of Oral Biology, University of Nebraska Medical Center, Lincoln, NE, USA.
Zhi LiDepartment of Oral Biology, University of Nebraska Medical Center, Lincoln, NE, USA.
Chunling WangShandong Provincial Key Laboratory of Oral Biomedicine, Department of Orthodontics, School of Stomatology, Shandong University, Jinan, Shandong, P.R. China.
Ali NawshadDepartment of Oral Biology, University of Nebraska Medical Center, Lincoln, NE, USA. Electronic address: Anawshad@unmc.edu.
University of Nebraska Medical Center · USShandong University · CN

Funding

Research Pilot Project ProgramP30GM106397 · NIGMS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI JOHNSON, KEITH R · 2013 to 2017
$4.9M
TGFbeta3 SIGNALING IN DEVELOPMENT OF PALATER01DE017986 · NIDCR · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI NAWSHAD, ALI · 2008 to 2012
$1.8M
NIDCR NIH HHS R01 DE017986NIGMS NIH HHS P30 GM106397
6 · The paper itself

Abstract

objectiveDuring the development of oral squamous cell carcinoma (OSCC), the transformed epithelial cells undergo increased proliferation resulting in tumor growth and invasion. Interestingly, throughout all phases of differentiation and progression to OSCC, transforming growth factor-β1 (TGF)-β1 induces cell cycle arrest or apoptosis; however, the role of TGF-β1 in promoting cancer cell proliferation has not been explored in detail. The purpose of this study was to identify the effect of TGF-β1 on OSCC cell proliferation. STUDY

designUsing both human OSCC samples and cell lines (UMSCC38 and UMSCC11B), we assessed protein, mRNA, gene expression, and protein-DNA interactions during OSCC progression.

resultsOur results showed that TGF-β1 increased OSCC cell proliferation by upregulating the expression of ΔNp63 and c-Myc oncogenes. Although the basal OSCC cell proliferation is sustained by activating ΔNp63, increased induction of c-Myc causes unregulated OSCC cell proliferation. Following induction of the cell cycle by ΔNp63 and c-Myc, cancer cells that halt c-Myc activity undergo epithelial mesenchymal transition or invasion while those that continue to express ΔNp63/c-Myc undergo unlimited progression through the cell cycle.

conclusionsOSCC proliferation is manifested by the induction of c-Myc in response to TGF-β1 signaling, which is essential for OSCC growth. Our data highlight the potential role of TGF-β1 in the induction of cancer progression and invasion of OSCC.

Indexed as

Blotting, WesternCarcinoma, Squamous CellCell Line, TumorCell MovementCell ProliferationDisease ProgressionEpithelial-Mesenchymal TransitionFlow CytometryHumansMouth NeoplasmsNeoplasm GradingProto-Oncogene Proteins c-mycSignal TransductionTranscription FactorsTransforming Growth Factor beta1Tumor Suppressor ProteinsMYC protein, humanProto-Oncogene Proteins c-mycTP63 protein, humanTranscription FactorsTransforming Growth Factor beta1Tumor Suppressor Proteins

Identifiers

PMID27567435
PMCPMC5892788
OpenAlexW2415007747

What OpenQuestion holds

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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.