Evidence map›Paper›PMID 33826094›Full record

ArticleGenes & genomics2021

Wnt5a-induced docking of Plk1 on HEF1 promotes HEF1 translocation and tumorigenesis.

Jeong-Ah Hwang, Ji Eun Yu, Sun-Ok Kim, Dong Hyun Kim, Kyoung Sang Cho, Kyung Ho Lee

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In one paragraph

Article in Genes & genomics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.1field-weighted citation impact, top 58% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. Article
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

6 authors at 4 institutions in 1 country.

Jeong-Ah Hwang *Anticancer Agent Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), 30 Yeongudanji-ro, Ochang, Cheongwon, Chungbuk, 28116, South Korea.
Ji Eun Yu *Anticancer Agent Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), 30 Yeongudanji-ro, Ochang, Cheongwon, Chungbuk, 28116, South Korea.
Sun-Ok KimAnticancer Agent Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), 30 Yeongudanji-ro, Ochang, Cheongwon, Chungbuk, 28116, South Korea.
Dong Hyun KimAnticancer Agent Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), 30 Yeongudanji-ro, Ochang, Cheongwon, Chungbuk, 28116, South Korea.
Kyoung Sang ChoDepartment of Biological Sciences, Konkuk University, 120 Neungdong-ro, Gwangjin-gu, Seoul, 05029, South Korea. kscho@konkuk.ac.kr.
Kyung Ho LeeAnticancer Agent Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), 30 Yeongudanji-ro, Ochang, Cheongwon, Chungbuk, 28116, South Korea. leekh@kribb.re.kr.ORCID 0000-0003-2587-775X
Korea Research Institute of Bioscience and Biotechnology · KRChungbuk National University · KRChungnam National University · KRKonkuk University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundUpregulation of human enhancer filamentation 1 (HEF1/NEDD9/Cas-L) and Polo-like kinase 1 (Plk1) is closely correlated with metastasis of human cancer. However, the mechanism by which the overexpression of HEF1 or Plk1 stimulates cancer metastasis and induces tumorigenesis remains enigmatic. In addition, the accumulation of HEF1 at the focal adhesion (FA) is known to be an essential event in cancer cell migration, but the mechanism of how HEF1 is targeted to the FA remains yet to be unveiled.

objectiveThis study was performed to elucidate the FA docking mechanism of HEF1 and to determine its effect on tumorigenesis.

methodsTo confirm the effect of the kinase on HEF1 translocation, various expression-knockdown stable cell lines were generated using a lentivirus system, and the effect of the HEF1-Plk1 complex on tumorigenesis was confirmed using a xenograft mouse model.

resultsHere, we show that Wnt5a-dependent Plk1 binding to HEF1 is critically required for HEF1 translocation to the FA. We also confirmed that Plk1 and CK1δ activities essential for HEF1 translocation are induced by Wnt5a. Finally, we confirmed the induction of tumorigenesis by the HEF1-Plk1 complex in the xenograft mouse model.

conclusionOur data collectively unveil the Wnt5a-CK1δ-HEF1-Plk1-FA remodeling pathway that governs HEF1 transportation to the FA to induce cell migration and tumorigenesis. This study sheds light on a mechanism underlying tumorigenesis and provides new strategies for anticancer therapy.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsCarcinogenesisCell Cycle ProteinsCell MovementHEK293 CellsHeLa CellsHumansMaleMiceMice, Inbred BALB CPolo-Like Kinase 1Protein Serine-Threonine KinasesProto-Oncogene ProteinsWnt-5a ProteinAdaptor Proteins, Signal TransducingCell Cycle ProteinsNEDD9 protein, humanPolo-Like Kinase 1Protein Serine-Threonine KinasesProto-Oncogene ProteinsWnt-5a ProteinWNT5A protein, humanFocal adhesionHEFPlk1TumorigenesisWnt5a

Identifiers

PMID33826094
OpenAlexW3151653841

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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.