ArticleThe Journal of biological chemistry2014
Liver kinase B1 expression promotes phosphatase activity and abrogation of receptor tyrosine kinase phosphorylation in human cancer cells.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 6 papers.
What it found
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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.
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- Combined effect of metformin and ezetimibe on PPAR-γ and adiponectin gene expression and biochemical parameters in MAFLD patients with type 2 diabetes.Scientific reports · 2025 · on this mapTrial
- Genome-wide CRISPR screens in spheroid culture reveal that the tumor suppressor LKB1 inhibits growth via the PIKFYVE lipid kinase.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Aberrant NRP-1 expression serves as predicator of metastatic endometrial and lung cancers.Oncotarget · 2016Article
- Neovascularization in the pulmonary endothelium is regulated by the endosome: Rab4-mediated trafficking and p18-dependent signaling.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- LKB1 in transmembrane receptor signaling.Oncotarget · 2015Article
- Inositol pyrophosphates promote tumor growth and metastasis by antagonizing liver kinase B1.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
Corrections and comments
- Correction · 2019-08-16Error in Image · Upgrade/Update of Prior Notice(s) ·
- Expression of concern · 2019-06-21Concerns/Issues about Data · Concerns/Issues about Results and/or Conclusions · Updated to Correction ·
- Erratum issued
- Expression of concern
Authors and funding
3 authors at 1 institution in 2 countries.
Funding
Abstract
Aberrant receptor tyrosine kinase phosphorylation (pRTK) has been associated with diverse pathological conditions, including human neoplasms. In lung cancer, frequent liver kinase B1 (LKB1) mutations correlate with tumor progression, but potential links with pRTK remain unknown. Heightened and sustained receptor activation was demonstrated by LKB1-deficient A549 (lung) and HeLaS3 (cervical) cancer cell lines. Depletion (siRNA) of endogenous LKB1 expression in H1792 lung cancer cells also correlated with increased pRTK. However, ectopic LKB1 expression in A549 and HeLaS3 cell lines, as well as H1975 activating-EGF receptor mutant lung cancer cell resulted in dephosphorylation of several tumor-enhancing RTKs, including EGF receptor, ErbB2, hepatocyte growth factor receptor (c-Met), EphA2, rearranged during transfection (RET), and insulin-like growth factor I receptor. Receptor abrogation correlated with attenuation of phospho-Akt and increased apoptosis. Global phosphatase inhibition by orthovanadate or depletion of protein tyrosine phosphatases (PTPs) resulted in the recovery of receptor phosphorylation. Specifically, the activity of SHP-2, PTP-1β, and PTP-PEST was enhanced by LKB1-expressing cells. Our findings provide novel insight on how LKB1 loss of expression or function promotes aberrant RTK signaling and rapid growth of cancer cells.
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Registered trials
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.