Evidence map›Paper›PMID 30796717›Full record

ArticleJournal of cell communication and signaling2019

CLDN10 promotes a malignant phenotype of osteosarcoma cells via JAK1/Stat1 signaling.

Xiaowei Zhang, Xianbin Wang, Aiyu Wang, Qian Li, Ming Zhou, Tao Li

Open access · bronzeAbstract read
In one paragraph

Article in Journal of cell communication and signaling, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

19 citing papers in PubMed, 26 citations in OpenAlex.

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  14. Long Noncoding RNACancer management and research · 2020
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  15. Article
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  18. Expression Patterns ofFrontiers in cell and developmental biology · 2020
    Article
  19. C-Terminus of E1A Binding Protein 1 Stimulates Malignant Phenotype in Human Hepatocellular Carcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2019
    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

6 authors at 1 institution in 1 country.

Xiaowei ZhangDepartment of Orthopedic Surgery, Central Hospital of Zibo, Affiliated with Shandong University, Gong qingtuan Road 54 Hao, Zibo, Shandong Province, China.
Xianbin WangDepartment of Orthopedic Surgery, Central Hospital of Zibo, Affiliated with Shandong University, Gong qingtuan Road 54 Hao, Zibo, Shandong Province, China.
Aiyu WangDepartment of Rehabilitation, Central Hospital of Zibo, Affiliated with Shandong University, Zibo, Shandong Province, China.
Qian LiDepartment of Orthopedic Surgery, Central Hospital of Zibo, Affiliated with Shandong University, Gong qingtuan Road 54 Hao, Zibo, Shandong Province, China.
Ming ZhouDepartment of Orthopedic Surgery, Central Hospital of Zibo, Affiliated with Shandong University, Gong qingtuan Road 54 Hao, Zibo, Shandong Province, China.
Tao LiDepartment of Orthopedic Surgery, Central Hospital of Zibo, Affiliated with Shandong University, Gong qingtuan Road 54 Hao, Zibo, Shandong Province, China. taolichina@126.com.ORCID http://orcid.org/0000-0003-4503-2543
Shandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In our previous study, the expression profile of tight junction (TJ) protein claudins (CLDNs) in human osteosarcoma (OS) cells was examined, and the data found the CLDN10 was high expressed in OS cells versus fetal osteoblast cells. Hence, we aim to determine the impacts and the molecular mechanisms of CLDN10 in the metastatic phenotype of OS. The exact expression profiles of CLDN10 and phosphorylated Janus kinase 1 (JAK1) in noncancerous bone tissues and OS tissues were detected via a western blotting and immunohistochemistry method. The OS cells with CLDN10 or JAK1 silencing was established via an RNA interference (RNAi) method, and an osteoblast cell line stably expressing CLDN10 was established via cell transfection. Then, the transfection effects and activation states of JAK1/ signal transducer and activator of transcription1 (Stat1) pathway in OS and osteoblast cells were detected via a western blotting assay. Moreover, the metastatic ability of osteoblast cells and OS cells in vitro were evaluated by means of a cell counting kit-8 (CCK8) assay, colony formation assay in soft agar, transwell assay and wound-healing experiment. The present data revealed that CLDN10 and phospho-JAK1 were up-regulated in OS tissues compared with noncancerous bone tissues. Genetic loss of CLDN10 or JAK1 inhibited the activation of the Stat1 and the malignant phenotype in OS cells. To sum up, our study suggested the CLDN10 enhanced the metastatic phenotype of OS cells via the activation of the JAK1/Stat1 signaling pathway.

Indexed as

Claudin-10Janus kinase 1MetastasisOsteosarcomaSignal transducer and activator of transcription1

Identifiers

PMID30796717
PMCPMC6732137
OpenAlexW2916957850

What OpenQuestion holds

Textmetadata
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.