Evidence map›Paper›PMID 35130902›Full record

ArticleBMC medicine2022

Upregulation of NOD1 and NOD2 contribute to cancer progression through the positive regulation of tumorigenicity and metastasis in human squamous cervical cancer.

Yuanyuan Zhang, Ning Li, Guangwen Yuan, Hongwen Yao, Die Zhang, Nan Li, Gongyi Zhang, Yangchun Sun, Wenpeng Wang, Jia Zeng and 3 more

Open access · goldAbstract read
In one paragraph

Article in BMC medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

24 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
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  9. Article
  10. The cancer microbiome.Advances in clinical chemistry · 2025
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Role and molecular mechanism of NOD2 in chronic non-communicable diseases.Journal of molecular medicine (Berlin, Germany) · 2024
    Review
  16. Review
  17. Article
  18. Harnessing innate immune pathways for therapeutic advancement in cancer.Signal transduction and targeted therapy · 2024
    Review
  19. Article
  20. Article
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

13 authors at 1 institution in 1 country.

Yuanyuan ZhangDepartment of Gynecologic Oncology, National Cancer Center/ National Clinical Research Center for Cancer/ Cancer Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Panjiayuan, Chaoyang District, 100021, Beijing, People's Republic of China.
Ning LiDepartment of Gynecologic Oncology, National Cancer Center/ National Clinical Research Center for Cancer/ Cancer Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Panjiayuan, Chaoyang District, 100021, Beijing, People's Republic of China.
Guangwen YuanDepartment of Gynecologic Oncology, National Cancer Center/ National Clinical Research Center for Cancer/ Cancer Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Panjiayuan, Chaoyang District, 100021, Beijing, People's Republic of China.
Hongwen YaoDepartment of Gynecologic Oncology, National Cancer Center/ National Clinical Research Center for Cancer/ Cancer Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Panjiayuan, Chaoyang District, 100021, Beijing, People's Republic of China.
Die ZhangLaboratory of Cell and Molecular Biology & State Key Laboratory of Molecular Oncology, National Cancer Center/ National Clinical Research Center for Cancer/ Cancer Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Panjiayuan, Chaoyang District, 100021, Beijing, People's Republic of China.
Nan LiDepartment of Gynecologic Oncology, National Cancer Center/ National Clinical Research Center for Cancer/ Cancer Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Panjiayuan, Chaoyang District, 100021, Beijing, People's Republic of China.
Gongyi ZhangDepartment of Gynecologic Oncology, National Cancer Center/ National Clinical Research Center for Cancer/ Cancer Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Panjiayuan, Chaoyang District, 100021, Beijing, People's Republic of China.
Yangchun SunDepartment of Gynecologic Oncology, National Cancer Center/ National Clinical Research Center for Cancer/ Cancer Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Panjiayuan, Chaoyang District, 100021, Beijing, People's Republic of China.
Wenpeng WangDepartment of Gynecologic Oncology, National Cancer Center/ National Clinical Research Center for Cancer/ Cancer Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Panjiayuan, Chaoyang District, 100021, Beijing, People's Republic of China.
Jia ZengDepartment of Gynecologic Oncology, National Cancer Center/ National Clinical Research Center for Cancer/ Cancer Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Panjiayuan, Chaoyang District, 100021, Beijing, People's Republic of China.
Ningzhi XuLaboratory of Cell and Molecular Biology & State Key Laboratory of Molecular Oncology, National Cancer Center/ National Clinical Research Center for Cancer/ Cancer Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Panjiayuan, Chaoyang District, 100021, Beijing, People's Republic of China.
Mei LiuLaboratory of Cell and Molecular Biology & State Key Laboratory of Molecular Oncology, National Cancer Center/ National Clinical Research Center for Cancer/ Cancer Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Panjiayuan, Chaoyang District, 100021, Beijing, People's Republic of China. liumei@cicams.ac.cn.
Lingying WuDepartment of Gynecologic Oncology, National Cancer Center/ National Clinical Research Center for Cancer/ Cancer Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Panjiayuan, Chaoyang District, 100021, Beijing, People's Republic of China. wulingying@csco.org.cn.
Chinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMetastatic cervical squamous cell carcinoma (CSCC) has poor prognosis and is recalcitrant to the current treatment strategies, which warrants the necessity to identify novel prognostic markers and therapeutic targets. Given that CSCC is a virus-induced malignancy, we hypothesized that the pattern recognition receptors (PRRs) involved in the innate immune response likely play a critical role in tumor development.

methodsA bioinformatics analysis, qPCR, IHC, immunofluorescence, and WB were performed to determine the expression of NOD1/NOD2. The biological characteristics of overexpression NOD1 or NOD2 CSCC cells were compared to parental cells: proliferation, migration/invasion and cytokines secretion were examined in vitro through CCK8/colony formation/cell cycle profiling/cell counting, wound healing/transwell, and ELISA assays, respectively. The proliferative and metastatic capacity of overexpression NOD1 or NOD2 CSCC cells were also evaluated in vivo. FCM, mRNA and protein arrays, ELISA, and WB were used to identify the mechanisms involved, while novel pharmacological treatment were evaluated in vitro and in vivo. Quantitative variables between two groups were compared by Student's t test (normal distribution) or Mann-Whitney U test (non-normal distribution), and one-way or two-way ANOVA was used for comparing multiple groups. Pearson χ

resultsNOD1 was highly expressed in CSCC with lymph-vascular space invasion (LVSI, P < 0.01) and lymph node metastasis (LM, P < 0.01) and related to worse overall survival (OS, P = 0.016). In vitro and in vivo functional assays revealed that the upregulation of NOD1 or NOD2 in CSCC cells promoted proliferation, invasion, and migration. Mechanistically, NOD1 and NOD2 exerted their oncogenic effects by activating NF-κb and ERK signaling pathways and enhancing IL-8 secretion. Inhibition of the IL-8 receptor partially abrogated the effects of NOD1/2 on CSCC cells.

conclusionsNOD1/2-NF-κb/ERK and IL-8 axis may be involved in the progression of CSCC; the NOD1 significantly enhanced the progression of proliferation and metastasis, which leads to a poor prognosis. Anti-IL-8 was identified as a potential therapeutic target for patients with NOD1

Indexed as

Carcinoma, Squamous CellNod1 Signaling Adaptor ProteinNod2 Signaling Adaptor ProteinUterine Cervical NeoplasmsFemaleHumansImmunity, InnateLymphatic MetastasisUp-RegulationNOD1 protein, humanNod1 Signaling Adaptor ProteinNOD2 protein, humanNod2 Signaling Adaptor ProteinCervical squamous cell carcinomaIL-8MetastasisNOD1/2Tumorigenicity

Identifiers

PMID35130902
PMCPMC8822783
OpenAlexW4210938880

What OpenQuestion holds

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LicenceCC BY
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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.