Evidence map›Paper›PMID 36653376›Full record

ArticleCell death & disease2023

Increased endogenous PKG I activity attenuates EGF-induced proliferation and migration of epithelial ovarian cancer via the MAPK/ERK pathway.

Ting Lan, Ying Li, Yue Wang, Zhong-Cheng Wang, Chun-Yan Mu, Ai-Bin Tao, Jian-Li Gong, Yuan Zhou, Hao Xu, Shi-Bao Li and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
6.0field-weighted citation impact, top 4% 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

17 citing papers in PubMed, 22 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

13 authors at 4 institutions in 2 countries.

Ting Lan *Xuzhou Key Laboratory of Laboratory Diagnostics, Xuzhou Medical University, Xuzhou City, Jiangsu Province, China.
Ying Li *Department of Laboratory Medicine, Affiliated Hospital of Xuzhou Medical University, Xuzhou City, Jiangsu Province, China.
Yue WangSchool of Medical Technology, Xuzhou Medical University, Xuzhou City, Jiangsu Province, China.
Zhong-Cheng WangXuzhou Key Laboratory of Laboratory Diagnostics, Xuzhou Medical University, Xuzhou City, Jiangsu Province, China.ORCID 0000-0001-8971-7742
Chun-Yan MuSchool of Medical Technology, Xuzhou Medical University, Xuzhou City, Jiangsu Province, China.
Ai-Bin TaoDivision of Cardiology, Department of Medicine, The Affiliated People's Hospital of Jiangsu University, Zhenjiang, China.
Jian-Li GongPerlmutter Cancer Center and Department of Surgery, NYU Langone Health, New York, NY, USA.
Yuan ZhouXuzhou Key Laboratory of Laboratory Diagnostics, Xuzhou Medical University, Xuzhou City, Jiangsu Province, China.
Hao XuDepartment of Gynecology Huangshi Love & Health Hospital affiliated to Hubei Polytechnic University, Hubei City, Wuhan Province, China.
Shi-Bao LiXuzhou Key Laboratory of Laboratory Diagnostics, Xuzhou Medical University, Xuzhou City, Jiangsu Province, China.ORCID 0000-0002-4026-4508
Bing GuXuzhou Key Laboratory of Laboratory Diagnostics, Xuzhou Medical University, Xuzhou City, Jiangsu Province, China.
Ping MaXuzhou Key Laboratory of Laboratory Diagnostics, Xuzhou Medical University, Xuzhou City, Jiangsu Province, China. pingm62@aliyun.com.
Lan LuoXuzhou Key Laboratory of Laboratory Diagnostics, Xuzhou Medical University, Xuzhou City, Jiangsu Province, China. luolan@xzhmu.edu.cn.ORCID 0000-0001-7549-9852
Xuzhou Medical College · CNHubei Polytechnic University · CNJiangsu University · CNNYU Langone Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The type I cGMP-dependent protein kinase (PKG I) is recognized as a tumor suppressor, but its role in EGFR regulated epithelial ovarian cancer (EOC) progression remains unclear. We evaluated the in vivo and in vitro effects of activated PKG I in EGF-induced EOC cell proliferation, migration, and invasion. The expressions of EGFR and PKG I were elevated, but the activated PKG I was decreased in EOC tissues of patients and cells lines. The addition of 8-Br-cGMP, a specific PKG I activator, attenuated the EGF-induced EOC cell proliferation, migration, and invasion in vitro. Similarly, activated PKG I also attenuated EOC progression in vivo using an EOC xenograft nude mouse model. The activated PKG I interacted with EGFR, causing increased threonine (693) phosphorylation and decreased tyrosine (1068) phosphorylation of EGFR, which resulted in disrupted EGFR-SOS1-Grb2 combination. Subsequently, the cytoplasmic phosphorylation of downstream proteins (c-Raf, MEK1/2, and ERK1/2) were declined, impeding the phosphorylated ERK1/2's nucleus translocation, and this reduction of phosphorylated tyrosine (1068) EGFR and ERK1/2 were also abolished by Rp-8-Br-cGMPS. Our results suggest that the activation of PKG I attenuates EGF-induced EOC progression, and the 8-Br-cGMP-PKG I-EGFR/MEK/ERK axis might be a potential target for EOC therapy.

Indexed as

MAP Kinase Signaling SystemOvarian NeoplasmsAnimalsCarcinoma, Ovarian EpithelialCell Line, TumorCell ProliferationCyclic GMPEpidermal Growth FactorErbB ReceptorsFemaleHumansMicePhosphorylationThionucleotidesTyrosine8-bromoguanosino-3',5'-cyclic monophosphorothioateCyclic GMPEpidermal Growth FactorErbB ReceptorsThionucleotidesTyrosine

Identifiers

PMID36653376
PMCPMC9849337
OpenAlexW4317370018

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.