Evidence map›Paper›PMID 32822099›Full record

ArticleJournal of clinical laboratory analysis2020

COLEC12 regulates apoptosis of osteosarcoma through Toll-like receptor 4-activated inflammation.

Guang-Zhang Li, Jian-Feng Deng, Ying-Zhao Qi, Ran Liu, Zhi-Xin Liu

Open access · goldAbstract read
In one paragraph

Article in Journal of clinical laboratory analysis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

21 citing papers in PubMed, 26 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

5 authors at 1 institution in 1 country.

Guang-Zhang LiDepartment of Orthopedics, the First Hospital of Qinhuangdao, Hebei, China.ORCID https://orcid.org/0000-0002-3200-3762
Jian-Feng DengDepartment of Orthopedics, the First Hospital of Qinhuangdao, Hebei, China.
Ying-Zhao QiDepartment of Orthopedics, the First Hospital of Qinhuangdao, Hebei, China.
Ran LiuDepartment of Orthopedics, the First Hospital of Qinhuangdao, Hebei, China.
Zhi-Xin LiuDepartment of Orthopedics, the First Hospital of Qinhuangdao, Hebei, China.
First Hospital of Qinhuangdao · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo investigate the role of COLEC12 in osteosarcoma and observe the relationship between COLEC12 knockdown and the inflammation of osteosarcoma. Then, further explore whether the process is regulated by TLR4.

methodGEPIA and TCGA systems were used to predict the potential function of COLEC12. Western blot and RT-PCR were used to analyze the protein expression, or mRNA level, of COLEC12 in different tissue or cell lines. The occurrence and development of osteosarcoma were observed by using COLEC12 knockdown lentivirus. The inflammation indexes of osteosarcoma, in vitro and in vivo, were explored. TLR4 knockdown lentivirus was applied to the relationship between COLEC12 and TLR4.

resultsCOLEC12 expression in SARC tumor tissue was higher than in normal, and a high expression of COLEC12 in SARC patients had a worse prognostic outcome. Pairwise gene correlation analysis revealed a potential relationship between COLEC12 and TLR4. The COLEC12 expression and mRNA level in the tumor or Saos-2 cells were increased. COLEC12 knockdown lentivirus could inhibit osteosarcoma development, in vivo and vitro, through reducing tumor volume and weight, weakening tumor proliferation, migration, and invasion, and enhancing apoptosis. Furthermore, COLEC12 knockdown could increase inflammation of osteosarcoma, in vivo and in vitro, through inducing myeloperoxidase (MPO), TLR4, NF-κB, and C3, and expression of related inflammatory factors. Finally, TLR4 knockdown lentivirus inhibits the progress of inflammation after COLEC12 regulation, in vivo and vitro.

conclusionCOLEC12 may be able to regulate apoptosis and inflammation of osteosarcoma, and TLR4 may be the downstream target factor of COLEC12 in inflammation.

Indexed as

CollectinsReceptors, ScavengerToll-Like Receptor 4AnimalsApoptosisCell Line, TumorGene Knockdown TechniquesHumansInflammationMiceMice, Inbred BALB COsteosarcomaCOLEC12 protein, humanCollectinsReceptors, ScavengerTLR4 protein, humanToll-Like Receptor 4COLEC12inflammationosteosarcomaTLR4

Identifiers

PMID32822099
PMCPMC7676208
OpenAlexW3080495272

What OpenQuestion holds

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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.