Evidence map›Paper›PMID 31822797›Full record

ArticleOncogene2020

Plakophilin 1 enhances MYC translation, promoting squamous cell lung cancer.

Joel Martin-Padron, Laura Boyero, Maria Isabel Rodriguez, Alvaro Andrades, Inés Díaz-Cano, Paola Peinado, Carlos Baliñas-Gavira, Juan Carlos Alvarez-Perez, Isabel F Coira, María Esther Fárez-Vidal and 1 more

Erratum issuedAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.5field-weighted citation impact, top 17% 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, 31 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 1 country.

Joel Martin-Padron *Centre for Genomics and Oncological Research (GENYO), Granada, Spain.
Laura Boyero *Centre for Genomics and Oncological Research (GENYO), Granada, Spain.
Maria Isabel RodriguezCentre for Genomics and Oncological Research (GENYO), Granada, Spain.
Alvaro AndradesCentre for Genomics and Oncological Research (GENYO), Granada, Spain.
Inés Díaz-CanoCentre for Genomics and Oncological Research (GENYO), Granada, Spain.
Paola PeinadoCentre for Genomics and Oncological Research (GENYO), Granada, Spain.
Carlos Baliñas-GaviraCentre for Genomics and Oncological Research (GENYO), Granada, Spain.
Juan Carlos Alvarez-PerezCentre for Genomics and Oncological Research (GENYO), Granada, Spain.
Isabel F CoiraCentre for Genomics and Oncological Research (GENYO), Granada, Spain.
María Esther Fárez-VidalDepartment of Biochemistry and Molecular Biology III, University of Granada, Granada, Spain. efarez@ugr.es.
Pedro P MedinaCentre for Genomics and Oncological Research (GENYO), Granada, Spain. pedromedina@ugr.es.
Universidad de Granada · ESPfizer-University of Granada-Junta de Andalucía Centre for Genomics and Oncological Research · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Plakophilin 1 (PKP1) is a member of the arm-repeat (armadillo) and plakophilin gene families and it is an essential component of the desmosomes. Although desmosomes have generally been associated with tumor suppressor functions, we have consistently observed that PKP1 is among the top overexpressed proteins in squamous cell lung cancer. To explore this paradox, we developed in vivo and in vitro functional models of PKP1 gain/loss in squamous cell lung cancer. CRISPR-Cas9 PKP1 knockout severely impaired cell proliferation, but it increased cell dissemination. In addition, PKP1 overexpression increased cell proliferation, cell survival, and in vivo xenograft engraftment. We further investigated the molecular mechanism of the mainly oncogenic function of PKP1 by combining transcriptomics, proteomics, and protein-nucleic acid interaction assays. Interestingly, we found that PKP1 enhances MYC translation in collaboration with the translation initiation complex by binding to the 5'-UTR of MYC mRNA. We propose PKP1 as an oncogene in SqCLC and a novel posttranscriptional regulator of MYC. PKP1 may be a valuable diagnostic biomarker and potential therapeutic target for SqCLC. Importantly, PKP1 inhibition may indirectly target MYC, a primary anticancer target.

Identifiers

PMID31822797
OpenAlexW2995845574

What OpenQuestion holds

Textmetadata
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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.