Evidence map›Paper›PMID 30922366›Full record

ArticleJournal of experimental & clinical cancer research : CR2019

Sox11 promotes head and neck cancer progression via the regulation of SDCCAG8.

Junwei Huang, Eoon Hye Ji, Xinyuan Zhao, Li Cui, Kaori Misuno, Mian Guo, Zhigang Huang, Xiaohong Chen, Shen Hu

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.6field-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

25 citing papers in PubMed, 36 citations in OpenAlex.

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  18. Multi-Omics Analysis ofJournal of personalized medicine · 2021
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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

9 authors at 3 institutions in 2 countries.

Junwei HuangSchool of Dentistry, University of California, Los Angeles, CA, 90095, USA.
Eoon Hye JiSchool of Dentistry, University of California, Los Angeles, CA, 90095, USA.
Xinyuan ZhaoDepartment of Endodontics, Stomatological Hospital, Southern Medical University, Guangzhou, 510280, China.
Li CuiSchool of Dentistry, University of California, Los Angeles, CA, 90095, USA.
Kaori MisunoSchool of Dentistry, University of California, Los Angeles, CA, 90095, USA.
Mian GuoSchool of Dentistry, University of California, Los Angeles, CA, 90095, USA.
Zhigang HuangDepartment of Otorhinolaryngology, Key Laboratory of Otolaryngology Head and Neck Surgery, Beijing Tongren Hospital, Capital Medical University, Beijing, 100730, China.
Xiaohong ChenDepartment of Otorhinolaryngology, Key Laboratory of Otolaryngology Head and Neck Surgery, Beijing Tongren Hospital, Capital Medical University, Beijing, 100730, China.
Shen HuSchool of Dentistry, University of California, Los Angeles, CA, 90095, USA. shenhu@ucla.edu.
University of California, Los Angeles · USCapital Medical University · CNSouthern Medical University · CN

Funding

Tobacco-Related Disease Research Program 18XT-0114
6 · The paper itself

Abstract

backgroundSOX11 is a transcription factor that plays an important role in mantle cell lymphoma development. However, its functional role in head and neck squamous cell carcinoma (HNSCC) remains unknown.

methodsProtein expression was measured with Western blotting, immunohistochemistry or quantitative proteomics, and gene expression was measured with quantitative RT-PCR. Functional role of SOX11 in HNSCC was evaluated with MTS/apoptosis, migration, invasion assays and a xenograft model. A SOX11-targeting gene, SDCCAG8, was confirmed with chromatin immunoprecipitation (ChIP), luciferase reporter and rescue assays.

resultsSOX11 was up-regulated in recurrent versus primary HNSCC and in highly invasive versus low invasive HNSCC cell lines. Silencing SOX11 in HNSCC cell lines significantly inhibited the cell proliferation, migration, invasion and resistance to Cisplatin, and vice versa. Quantitative proteomic analysis of SOX11-silencing HNSCC cells revealed a number of differentially expressed proteins, including a down-regulated tumor antigen SDCCAG8. Silencing of SDCCAG8 in HNSCC cells also significantly inhibited the cell proliferation, migration and invasion, and vice versa. ChIP assays demonstrated that endogenous SOX11 strongly bound to Sdccag8 gene promoter in highly invasive HNSCC cells. When over-expressed in low invasive HNSCC cells, wild type SOX11 but not mutant SOX11 induced the promoter activity of Sdccag8 and significantly induced the expression of SDCCAG8. However, exogenous mutant SOX11 abolished the expression of SDCCAG8 in highly invasive HNSCC cells. In addition, the inhibitory effects of SOX11 knockdown were partially rescued by over-expression of SDCCAG8 in HNSCC cells.

conclusionCollectively, our findings indicate SOX11 promotes HNSCC progression via the regulation of SDCCAG8.

Indexed as

Up-RegulationAnimalsAutoantigensCarcinoma, Squamous CellCell Line, TumorCell MovementCell ProliferationDisease ProgressionGene Expression Regulation, NeoplasticHead and Neck NeoplasmsHumansMiceNeoplasm ProteinsNeoplasm TransplantationSOXC Transcription FactorsAutoantigensNeoplasm ProteinsSDCCAG8 protein, humanSOX11 protein, humanSOXC Transcription FactorsHead and neck squamous cell carcinomaInvasionProteomicsSDCCAG8SOX11

Identifiers

PMID30922366
PMCPMC6440126
OpenAlexW2887800014

What OpenQuestion 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 OpenQuestion graph.