Evidence map›Paper›PMID 32363163›Full record

ArticleFrontiers in oncology2020

FOXK1 Promotes Proliferation and Metastasis of Gallbladder Cancer by Activating AKT/mTOR Signaling Pathway.

Ma Wencong, Wang Jinghan, Yu Yong, Ao Jianyang, Li Bin, Cheng Qingbao, Liu Chen, Jiang Xiaoqing

Open access · goldAbstract read
In one paragraph

Article in Frontiers in oncology, 2020. 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
1.4field-weighted citation impact, top 19% 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, 26 citations in OpenAlex.

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  14. miR-217-5p Inhibits Invasion and Metastasis of Prostate Cancer by Targeting Clusterin.Mammalian genome : official journal of the International Mammalian Genome Society · 2021
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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

8 authors at 1 institution in 1 country.

Ma WencongDepartment of Biliary Tract Surgery I, Third Affiliated Hospital of Second Military Medical University, Shanghai, China.
Wang JinghanDepartment of Biliary Tract Surgery I, Third Affiliated Hospital of Second Military Medical University, Shanghai, China.
Yu YongDepartment of Biliary Tract Surgery I, Third Affiliated Hospital of Second Military Medical University, Shanghai, China.
Ao JianyangDepartment of Biliary Tract Surgery I, Third Affiliated Hospital of Second Military Medical University, Shanghai, China.
Li BinDepartment of Biliary Tract Surgery I, Third Affiliated Hospital of Second Military Medical University, Shanghai, China.
Cheng QingbaoDepartment of Biliary Tract Surgery I, Third Affiliated Hospital of Second Military Medical University, Shanghai, China.
Liu ChenDepartment of Biliary Tract Surgery I, Third Affiliated Hospital of Second Military Medical University, Shanghai, China.
Jiang XiaoqingDepartment of Biliary Tract Surgery I, Third Affiliated Hospital of Second Military Medical University, Shanghai, China.
Second Military Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gallbladder cancer (GBC) is one of the most lethal malignancies worldwide, with extremely poor prognosis. Recently, forkhead box k1 (FOXK1), a member of the FOX transcription factor family, has been reported to be correlated with tumor progression in multiple malignancies. However, the role of FOXK1 in GBC has not been elucidated. In this study, we demonstrated that the expression level of FOXK1 was elevated in human GBC tissues and associated with increased liver metastasis, poor histological differentiation, advanced TNM stage, and shorter overall survival. Knockdown of FOXK1 expression inhibited GBC cells proliferation and metastasis. Consistently, overexpression of FOXK1 promoted GBC cells progression. Mechanical investigations verified that knockdown of FOXK1 could lead to G1/S cell cycle arrest through downregulating CDK4, CDK6, cyclin D1, and cyclin E1. And FOXK1 could regulate the expression of epithelial-mesenchymal transition (EMT) related proteins E-cad, N-cad, and Vimentin. Moreover, we found that FOXK1 could regulate the activation of Akt/mTOR signaling pathway. In addition, AKT special inhibitor MK-2206 could abolish the proliferation and metastasis discrepancy between FOXK1 overexpression GBC cells and control cells, which suggested the tumorpromoting effect of FOXK1 may be partially related with the activations of Akt/mTOR signaling pathway. Collectively, our results suggested that FOXK1 promotes GBC cells progression and represent a novel prognostic biomarker and potential therapeutic target in GBC.

Indexed as

AKT/mTORFOXK1gallbladder cancerprognosisprogression

Identifiers

PMID32363163
PMCPMC7180204
OpenAlexW3016378278

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.