Evidence map›Paper›PMID 31118684›Full record

ArticleOncoTargets and therapy2019

Nicotine promotes cervical metastasis of oral cancer by regulating peroxiredoxin 1 and epithelial-mesenchymal transition in mice.

Min Wang, Wenwen Niu, Moci Qi, Hui Chen, Min Zhang, Chunxiao Wang, Lihua Ge, Jing Yang, Congcong Miao, Ni Shi and 2 more

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

Article in OncoTargets and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

10 citing papers in PubMed, 17 citations in OpenAlex.

  1. E-Cigarette effects on oral health: A molecular perspective.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2025
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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 3 institutions in 3 countries.

Min WangBeijing Institute of Dental Research, Beijing Stomatological Hospital and School of Stomatology, Capital Medical University, Beijing 100050, People's Republic of China, xftang10@ccmu.edu.cn.
Wenwen NiuBeijing Shibalidian Community Hospital, Beijing, People's Republic of China.
Moci QiBeijing Institute of Dental Research, Beijing Stomatological Hospital and School of Stomatology, Capital Medical University, Beijing 100050, People's Republic of China, xftang10@ccmu.edu.cn.
Hui ChenBeijing Institute of Dental Research, Beijing Stomatological Hospital and School of Stomatology, Capital Medical University, Beijing 100050, People's Republic of China, xftang10@ccmu.edu.cn.
Min ZhangBeijing Institute of Dental Research, Beijing Stomatological Hospital and School of Stomatology, Capital Medical University, Beijing 100050, People's Republic of China, xftang10@ccmu.edu.cn.
Chunxiao WangBeijing Institute of Dental Research, Beijing Stomatological Hospital and School of Stomatology, Capital Medical University, Beijing 100050, People's Republic of China, xftang10@ccmu.edu.cn.
Lihua GeBeijing Institute of Dental Research, Beijing Stomatological Hospital and School of Stomatology, Capital Medical University, Beijing 100050, People's Republic of China, xftang10@ccmu.edu.cn.
Jing YangBeijing Institute of Dental Research, Beijing Stomatological Hospital and School of Stomatology, Capital Medical University, Beijing 100050, People's Republic of China, xftang10@ccmu.edu.cn.
Congcong MiaoBeijing Institute of Dental Research, Beijing Stomatological Hospital and School of Stomatology, Capital Medical University, Beijing 100050, People's Republic of China, xftang10@ccmu.edu.cn.
Ni ShiDivision of Medical Oncology, Department of Internal Medicine, The Arthur G. James Cancer Hospital and Richard J. Solove Research Institute, The Ohio State University, Columbus, OH 43210, USA, tong.chen@osumc.edu.
Tong ChenDivision of Medical Oncology, Department of Internal Medicine, The Arthur G. James Cancer Hospital and Richard J. Solove Research Institute, The Ohio State University, Columbus, OH 43210, USA, tong.chen@osumc.edu.
Xiaofei TangBeijing Institute of Dental Research, Beijing Stomatological Hospital and School of Stomatology, Capital Medical University, Beijing 100050, People's Republic of China, xftang10@ccmu.edu.cn.
Capital Medical University · CNThe Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute · USBeijing Haidian Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTobacco is a major risk factor for oral squamous cell carcinoma (OSCC). However, the role of nicotine in OSCC is not completely understood. MATERIALS AND

methodsTo analyze the mechanisms of nicotine-induced cervical metastasis, we investigated whether nicotine induced invasion, migration, and epithelial-mesenchymal transition (EMT) via regulating peroxiredoxin 1 (Prx1) in CAL 27 cells. In addition, we established a mouse model to confirm the roles of nicotine in regulating Ets1/Prx1/EMT signaling in OSCC metastasis.

resultsWe showed that nicotine induced CAL 27 cell invasion, migration, EMT, and Prx1 and Ets1 expression. Prx1 knockdown inhibited cell invasion, migration, and EMT. Ets1 silencing downregulated Prx1 expression and EMT. Prx1 and Ets1 were shown to interact in CAL 27 cells treated with nicotine, and nicotine could significantly upregulate the binding of the transcription factor Ets1 to the Prx1 gene promoter region. Additionally, an in vivo study showed that nicotine induced tumor metastasis and EMT. Prx1 knockdown inhibited cervical metastasis rates and EMT progression. No significant differences in metastasis rates and EMT-related marker expression levels were observed between vehicle- and nicotine-treated mice.

conclusionThe results indicate that nicotine promotes cervical lymph node metastasis through regulating Ets1/Prx1/EMT signaling during OSCC pathogenesis; consequently, Prx1 may represent a potential target for the prevention and treatment of OSCC.

Indexed as

epithelial-mesenchymal transitionmetastasismouse modeloral squamous cell carcinomaperoxiredoxin 1

Identifiers

PMID31118684
PMCPMC6501726
OpenAlexW2942909746

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.