Evidence map›Paper›PMID 30038287›Full record

ArticleCell death & disease2018

Overexpression of PEAK1 contributes to epithelial-mesenchymal transition and tumor metastasis in lung cancer through modulating ERK1/2 and JAK2 signaling.

Chenbo Ding, Wendong Tang, Xiaobo Fan, Xiyong Wang, Hairu Wu, Hongbo Xu, Wei Xu, Wei Gao, Guoqiu Wu

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

33 citing papers in PubMed, 57 citations in OpenAlex.

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  8. Role of microRNA-363 during tumor progression and invasion.Journal of physiology and biochemistry · 2024
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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

9 authors at 2 institutions in 1 country.

Chenbo DingMedical School of Southeast University, Nanjing, 210009, China. dcb06296632@163.com.
Wendong TangMedical School of Southeast University, Nanjing, 210009, China.
Xiaobo FanMedical School of Southeast University, Nanjing, 210009, China.
Xiyong WangMedical School of Southeast University, Nanjing, 210009, China.
Hairu WuMedical School of Southeast University, Nanjing, 210009, China.
Hongbo XuMedical School of Southeast University, Nanjing, 210009, China.
Wei XuMedical School of Southeast University, Nanjing, 210009, China.
Wei GaoCenter of Clinical Laboratory Medicine, Zhongda Hospital, Southeast University, Nanjing, 210009, China.
Guoqiu WuMedical School of Southeast University, Nanjing, 210009, China. nationball@163.com.
Southeast University · CNZhongda Hospital Southeast University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pseudopodium-enriched atypical kinase 1 (PEAK1), a novel non-receptor tyrosine kinase, has been demonstrated to act as an oncogenic regulator in breast and pancreatic cancers. However, the role of PEAK1 in the progression and metastasis of lung cancer is still unknown. Here, we observed that ectopic PEAK1 expression promoted lung cancer cell migration and invasion, while PEAK1 knockout resulted in suppressed cell migration and invasion. Interestingly, cell proliferation did not significantly increase or decrease in either the PEAK1 overexpression or knockout groups compared with the corresponding control cells. In addition, PEAK1 overexpression could induce epithelial-to-mesenchymal transition (EMT) and the expression of matrix metalloproteinase-2 (MMP2) and MMP9 both in vitro and in vivo, whereas PEAK1 knockout had the opposite effects. Then, we had confirmed that PEAK1 was significantly upregulated in lung cancer tissues, and correlated with a higher tumor node metastasis stage. Moreover, PEAK1 upregulation markedly enhanced the activation of extracellular signal-regulated kinase-1/2 (ERK1/2) and Janus kinase-2 (JAK2) signaling in lung cancer cells. Further work demonstrated that the combination of PD98059 with AZD1480 could reverse the effects of PEAK1-induced EMT, cell migration and invasion. Our findings highlight a newer mechanism for PEAK1 in regulating EMT and metastasis in lung cancer, which might serve as a therapeutic target for lung cancer patients.

Indexed as

AnimalsCarcinoma, Non-Small-Cell LungCell Line, TumorCell MovementEpithelial-Mesenchymal TransitionFemaleFlavonoidsHumansJanus Kinase 2Lung NeoplasmsMaleMatrix Metalloproteinase 2Matrix Metalloproteinase 9MiceMice, NudeMiddle Aged2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-oneFlavonoidsJAK2 protein, humanJanus Kinase 2Matrix Metalloproteinase 2Matrix Metalloproteinase 9Mitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3PEAK1 protein, humanProtein-Tyrosine Kinases

Identifiers

PMID30038287
PMCPMC6056550
OpenAlexW2884980342

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.