Evidence map›Paper›PMID 29039489›Full record

ArticleMolecular medicine reports2017

ID1 contributes to cell growth invasion and migration in salivary adenoid cystic carcinoma.

Xiao-Meng Hu, Ting Lin, Xiao-Yu Huang, Rui-Huan Gan, Yong Zhao, Yan Feng, Lin-Can Ding, Bo-Hua Su, Da-Li Zheng, You-Guang Lu

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

5 citing papers in PubMed, 14 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

10 authors at 1 institution in 1 country.

Xiao-Meng HuDepartment of Preventive Dentistry, The Affiliated Stomatological Hospital, Fujian Medical University, Fuzhou, Fujian 350002, P.R. China.
Ting LinDepartment of Preventive Dentistry, The Affiliated Stomatological Hospital, Fujian Medical University, Fuzhou, Fujian 350002, P.R. China.
Xiao-Yu HuangDepartment of Preventive Dentistry, The Affiliated Stomatological Hospital, Fujian Medical University, Fuzhou, Fujian 350002, P.R. China.
Rui-Huan GanDepartment of Preventive Dentistry, The Affiliated Stomatological Hospital, Fujian Medical University, Fuzhou, Fujian 350002, P.R. China.
Yong ZhaoDepartment of Pathology, The Affiliated Stomatological Hospital, Fujian Medical University, Fuzhou, Fujian 350002, P.R. China.
Yan FengDepartment of Preventive Dentistry, The Affiliated Stomatological Hospital, Fujian Medical University, Fuzhou, Fujian 350002, P.R. China.
Lin-Can DingDepartment of Preventive Dentistry, The Affiliated Stomatological Hospital, Fujian Medical University, Fuzhou, Fujian 350002, P.R. China.
Bo-Hua SuDepartment of Preventive Dentistry, The Affiliated Stomatological Hospital, Fujian Medical University, Fuzhou, Fujian 350002, P.R. China.
Da-Li ZhengKey Laboratory of Ministry of Education for Gastrointestinal Cancer, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, Fujian 350108, P.R. China.
You-Guang LuDepartment of Preventive Dentistry, The Affiliated Stomatological Hospital, Fujian Medical University, Fuzhou, Fujian 350002, P.R. China.
Fujian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previous studies have reported that inhibitor of DNA binding 1 (ID1) exerts an oncogenic role in a number of tumors. In the present study, the role of ID1 in the growth, invasion and migration of salivary adenoid cystic carcinoma (SACC) cells was investigated. ID1 expression in clinical SACC samples was compared with that in normal salivary tissues using immunohistochemical staining, and the correlation between ID1 expression and clinical pathological characteristics was then determined. Subsequently, ID1 was overexpressed or silenced to investigate the effects of ID1 expression on SACC cell proliferation, invasion and migration. In addition, the gene expression levels of known ID1 target genes, including S100A9, CDKN2A and matrix metalloproteinase 1 (MMP1) was measured using reverse transcription‑quantitative polymerase chain reaction to elucidate the potential mechanisms of ID1 in SACC. The results of the present study indicated that the protein expression levels of ID1 were significantly increased in the SACC tissues compared with that in the normal salivary tissues (P<0.001), and a positive correlation between ID1 expression and tumor stage (P=0.001), tumor invasion (P=0.002) and metastasis (P=0.019) in SACC was observed. Knockdown of ID1 in SACC cells significantly inhibited cell growth, invasion and migration (all P<0.01), whereas overexpression of ID1 promoted cell proliferation, invasion and migration (all P<0.01). The gene expression level of MMP1 was significantly reduced following ID1 knockdown in SACC‑83 cells when compared with negative controls (P<0.05), whereas S100A9 and CDKN2A expression levels were significantly upregulated (both P<0.05). The results suggest that ID1 may regulate the growth, invasion and migration of SACC cells, and that MMP1, S100A9 and CDKN2A may serve as target genes of ID1 and mediate the effects of ID1 in SACC cells. Therefore, ID1 may present a potential target gene for the treatment of patients with SACC to inhibit cancer cell growth and metastasis.

Indexed as

AdultAgedCarcinoma, Adenoid CysticCell Line, TumorCell MovementCell ProliferationFemaleGene ExpressionGene Knockdown TechniquesGenes, p16HumansInhibitor of Differentiation Protein 1MaleMatrix Metalloproteinase 1Middle AgedNeoplasm InvasivenessID1 protein, humanInhibitor of Differentiation Protein 1Matrix Metalloproteinase 1

Identifiers

PMID29039489
PMCPMC5779972
OpenAlexW2763021610

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Registered trials

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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.