Evidence map›Paper›PMID 27377307›Full record

ArticleScientific reports2016

Knockdown of Pentraxin 3 suppresses tumorigenicity and metastasis of human cervical cancer cells.

Tsung-Ho Ying, Chien-Hsing Lee, Hui-Ling Chiou, Shun-Fa Yang, Chu-Liang Lin, Chia-Hung Hung, Jen-Pi Tsai, Yi-Hsien Hsieh

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
3.6field-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

50 citing papers in PubMed, 86 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Role of long pentraxin PTX3 in cancer.Clinical and experimental medicine · 2023
    Review
  18. Article
  19. Review
  20. Review
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

8 authors at 4 institutions in 1 country.

Tsung-Ho YingDepartment of Obstetrics and Gynecology, Chung Shan Medical University Hospital, Taichung, Taiwan.
Chien-Hsing LeeSchool of Chinese Medicine, College of Chinese Medicine, China Medical University, Taichung, Taiwan.
Hui-Ling ChiouSchool of Medical Laboratory and Biotechnology, Chung Shan Medical University, Taichung, Taiwan.
Shun-Fa YangInstitute of Medicine, Chung Shan Medical University, Taichung, Taiwan.
Chu-Liang LinInstitute of Biochemistry, Microbiology and Immunology, Chung Shan Medical University, Taichung, Taiwan.
Chia-Hung HungInstitute of Biochemistry, Microbiology and Immunology, Chung Shan Medical University, Taichung, Taiwan.
Jen-Pi TsaiSchool of Medicine, Tzu Chi University, Hualien, Taiwan.
Yi-Hsien HsiehInstitute of Biochemistry, Microbiology and Immunology, Chung Shan Medical University, Taichung, Taiwan.
Chung Shan Medical University · TWChina Medical University · TWChung Shan Medical University Hospital · TWTzu Chi University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pentraxin 3 (PTX3) as an inflammatory molecule has been shown to be involved in immune response, inflammation, and cancer. However, the effects of PTX3 on the biological features of cervical cancer cells in vitro and in vivo have not been delineated. Immunohistochemical staining showed that increased PTX3 expression was significantly associated with tumor grade (P < 0.011) and differentiation (P < 0.019). Knocking down PTX3 with lentivirus-mediated small hairpin RNA (shRNA) in cervical cancer cell lines resulted in inhibited cell viability, diminished colony-forming ability, and induced cell cycle arrest at the G2/M phase of the cell cycle, along with downregulated expression of cyclin B1, cdc2, and cdc25c, and upregulated expression of p-cdc2, p-cdc25c, p21, and p27. Furthermore, knockdown of PTX3 significantly decreased the potential of migration and invasion of cervical cancer cells by inhibiting matrix metalloproteidase-2 (MMP-2), MMP-9, and urokinase plasminogen activator (uPA). Moreover, in vivo functional studies showed PTX3-knockdown in mice suppressed tumorigenicity and lung metastatic potential. Conversely, overexpression of PTX3 enhanced proliferation and invasion both in vitro and in vivo. Our results demonstrated that PTX3 contributes to tumorigenesis and metastasis of human cervical cancer cells. Further studies are warranted to demonstrate PTX3 as a novel therapeutic biomarker for human cervical cancer.

Indexed as

AdultAnimalsCell Line, TumorCell MovementCell ProliferationC-Reactive ProteinFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesHeLa CellsHumansLung NeoplasmsMaleMiceMiddle AgedNeoplasm GradingC-Reactive ProteinPentraxinsSerum Amyloid P-Component

Identifiers

PMID27377307
PMCPMC4932528
OpenAlexW2470057209

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.