Evidence map›Paper›PMID 31217475›Full record

ArticleCell death & disease2019

FBXO22 mediates polyubiquitination and inactivation of LKB1 to promote lung cancer cell growth.

Xiao-Na Zhu, Ping He, Liang Zhang, Shuo Yang, Hui-Lin Zhang, Di Zhu, Meng-Di Liu, Yun Yu

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

36 citing papers in PubMed, 68 citations in OpenAlex.

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  17. LKB1 biology: assessing the therapeutic relevancy of LKB1 inhibitors.Cell communication and signaling : CCS · 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

8 authors at 1 institution in 1 country.

Xiao-Na ZhuKey Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Rui-Jin hospital, Shanghai Jiao-Tong University School of Medicine (SJTU-SM), Shanghai, China.
Ping HeKey Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Rui-Jin hospital, Shanghai Jiao-Tong University School of Medicine (SJTU-SM), Shanghai, China.
Liang ZhangKey Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Rui-Jin hospital, Shanghai Jiao-Tong University School of Medicine (SJTU-SM), Shanghai, China.
Shuo YangKey Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Rui-Jin hospital, Shanghai Jiao-Tong University School of Medicine (SJTU-SM), Shanghai, China.
Hui-Lin ZhangKey Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Rui-Jin hospital, Shanghai Jiao-Tong University School of Medicine (SJTU-SM), Shanghai, China.
Di ZhuKey Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Rui-Jin hospital, Shanghai Jiao-Tong University School of Medicine (SJTU-SM), Shanghai, China.
Meng-Di LiuKey Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Rui-Jin hospital, Shanghai Jiao-Tong University School of Medicine (SJTU-SM), Shanghai, China.
Yun YuKey Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Rui-Jin hospital, Shanghai Jiao-Tong University School of Medicine (SJTU-SM), Shanghai, China. yy@shsmu.edu.cn.
Shanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Liver kinase B1 (LKB1) regulates both cell growth and energy metabolism. Inactivated mutations of LKB1, observed in 20-30% of nonsmall cell lung cancers (NSCLC), contribute significantly to lung cancer malignancy progression. However, the upstream signalings regulating LKB1 activity remain incompletely understood. Here, we present evidence that FBXO22 interacts with and promotes polyubiquitination of LKB1. More intriguingly, FBXO22 mediates Lys-63-linked LKB1 polyubiquitination and inhibits kinase activity of LKB1. Furthermore, over-expression of FBXO22 promotes NSCLC cell growth through inhibiting LKB1-AMPK-mTOR signaling in vitro and in vivo. Clinically, FBXO22 is highly expressed in human lung adenocarcinoma and high FBXO22 expression predicts significant poor prognosis. Our study provides new insights into the upstream regulation of LKB1 activation and identifies FBXO22 as a potential therapeutic target for lung cancer treatment.

Indexed as

A549 CellsAMP-Activated Protein Kinase KinasesAMP-Activated Protein KinasesAnimalsCarcinoma, Non-Small-Cell LungCell Line, TumorCell ProliferationColony-Forming Units AssayF-Box ProteinsFemaleHEK293 CellsHeLa CellsHumansImmunoblottingImmunohistochemistryImmunoprecipitationAMP-Activated Protein Kinase KinasesAMP-Activated Protein KinasesF-Box ProteinsFBXO22 protein, humanFbxo22 protein, mouseProtein Serine-Threonine KinasesReceptors, Cytoplasmic and NuclearSTK11 protein, humanStk11 protein, mouse

Identifiers

PMID31217475
PMCPMC6584689
OpenAlexW2949071566

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.