Evidence map›Paper›PMID 26755661›Full record

ArticleOncotarget2016

Axon guidance molecule semaphorin3A is a novel tumor suppressor in head and neck squamous cell carcinoma.

Zhao Wang, Jie Chen, Wei Zhang, Yang Zheng, Zilu Wang, Laikui Liu, Heming Wu, Jinhai Ye, Wei Zhang, Bing Qi and 2 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.0field-weighted citation impact, top 27% 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

11 citing papers in PubMed, 23 citations in OpenAlex.

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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

12 authors at 1 institution in 1 country.

Zhao WangJiangsu Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, 210029, China.
Jie ChenJiangsu Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, 210029, China.
Wei ZhangJiangsu Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, 210029, China.
Yang ZhengJiangsu Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, 210029, China.
Zilu WangJiangsu Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, 210029, China.
Laikui LiuJiangsu Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, 210029, China.
Heming WuJiangsu Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, 210029, China.
Jinhai YeJiangsu Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, 210029, China.
Wei ZhangDepartment of Oral Pathology, Affiliated Hospital of Stomatology, Nanjing Medical University, Nanjing, 210029, China.
Bing QiDepartment of Oral Pathology, Affiliated Hospital of Stomatology, Nanjing Medical University, Nanjing, 210029, China.
Yunong WuJiangsu Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, 210029, China.
Xiaomeng SongJiangsu Key Laboratory of Oral Diseases, Nanjing Medical University, Nanjing, 210029, China.
Nanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Semaphorin3A (SEMA3A), an axon guidance molecule in the nervous system, plays an inhibitory role in oncogenesis. Here, we investigated the expression pattern and biological roles of SEMA3A in head and neck squamous cell carcinoma (HNSCC) by gain-of-function assays using adenovirus transfection and recombinant human SEMA3A protein. In addition, we explored the therapeutic efficacy of SEMA3A against HNSCC in vivo. We found that lower expression of SEMA3A correlated with shorter overall survival and had independent prognostic importance in patients with HNSCC. Both genetic and recombinant SEMA3A protein inhibited cell proliferation and colony formation and induced apoptosis, accompanied by decreased cyclin E, cyclin D, CDK2, CDK4 and CDK6 and increased P21, P27, activated caspase-5 and caspase-7. Moreover, over-expression of SEMA3A suppressed migration, invasion and epithelial-to-mesenchymal transition due in part to the inhibition of NF-κB and SNAI2 in HNSCC cell lines. Furthermore, intratumoral SEMA3A delivery significantly stagnated tumor growth in a xenograft model. Taken together, our results indicate that SEMA3A serves as a tumor suppressor during HNSCC tumorigenesis and a new target for the treatment of HNSCC.

Indexed as

AnimalsAxon GuidanceCarcinoma, Squamous CellCell Line, TumorCell ProliferationFemaleGenes, Tumor SuppressorHead and Neck NeoplasmsHumansMaleMiceMice, Inbred BALB CMiddle AgedRandom AllocationSemaphorin-3ASquamous Cell Carcinoma of Head and NeckSEMA3A protein, humanSemaphorin-3AapoptosisHNSCCNF-kappaBsemaphorin3ASnail

Identifiers

PMID26755661
PMCPMC4868739
OpenAlexW2230809705

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.