Evidence map›Paper›PMID 33262655›Full record

ArticleCancer management and research2020

Extracellular Collagen Mediates Osteosarcoma Progression Through an Integrin α2β1/JAK/STAT3 Signaling Pathway.

Daiqing Wei, Cui Li, Junwu Ye, Feifan Xiang, Juncai Liu

Open access · goldAbstract read
In one paragraph

Article in Cancer management and research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

13 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Review
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  4. Promoting collagen synthesis: a viable strategy to combat skin ageing.Journal of enzyme inhibition and medicinal chemistry · 2025
    Review
  5. Article
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  12. Association of chondroadherin with leiomyosarcoma.Gynecologic oncology reports · 2023
    Article
  13. 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

5 authors at 1 institution in 1 country.

Daiqing WeiDepartment of Orthopaedics, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, People's Republic of China.
Cui LiDepartment of Nosocomial Infection Control, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, People's Republic of China.
Junwu YeDepartment of Orthopaedics, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, People's Republic of China.
Feifan XiangDepartment of Orthopaedics, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, People's Republic of China.
Juncai LiuDepartment of Orthopaedics, The Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, People's Republic of China.ORCID 0000-0002-8526-0076
Affiliated Hospital of Southwest Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOsteosarcoma development is a complex set which is determined by various factors. Many patients suffered from sustained osteosarcoma growth and revealed poor response to clinical interventions. However, the underlying mechanisms of osteosarcoma development still remain unclear.

methodsIn our study, we isolated osteosarcoma tissues from clinical patients, which were divided into high degree group (stage G1~G2) and low degree group (stage G0). The expression of type I collagen, integrin and STAT3 in tumor tissues were analyzed by immunohistochemistry or immunofluorescence. The collagen-induced cells proliferation was detected by CCK8 and colony formation analysis. The activation of JAK/STAT3 signal was examined by Western blotting and immunofluorescence. The anticancer effects of integrin α2β1 peptide were analyzed by Sao-2-bearing mice model.

resultsOur results implicated that type I collagen could facilitate malignant osteosarcoma development in patients. In vitro, 2D collagen culture also efficiently mediated the stemness up-regulation of osteosarcoma cells, resulting in the strengthened capability of cells proliferation and tumorigenesis. In mechanism, we found that type I collagen could facilitate the activation of JAK/STAT3 signals through integrin α2β1, which elicited tumor-sustained growth and cancer relapse. In tumor-bearing mice model, integrin α2β1 signals inhibitor significantly suppressed the osteosarcoma cells proliferation and their tumorigenic ability, which improved the outcome of chemotherapy/radiotherapy.

conclusionOur study demonstrated that type I collagen could mediate osteosarcoma development through an integrin α2β1/JAK/STAT3 signaling pathway. Blockade of integrin α2β1 by α2β1 inhibitor efficiently improved outcome of chemotherapy/radiotherapy, which provided new insights for eradicating tumors in clinic.

Indexed as

collagenintegrin α2β1JAK/STAT3osteosarcoma

Identifiers

PMID33262655
PMCPMC7699996
OpenAlexW3106702999

What OpenQuestion holds

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LicenceCC BY-NC
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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.