Evidence map›Paper›PMID 35439973›Full record

ArticleBMC cancer2022

Activated TAZ induces liver cancer in collaboration with EGFR/HER2 signaling pathways.

Hyuk Moon, Hyunjung Park, Min Jee Chae, Hye Jin Choi, Do Young Kim, Simon Weonsang Ro

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

16 citing papers in PubMed, 22 citations in OpenAlex.

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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

6 authors at 3 institutions in 1 country.

Hyuk MoonDepartment of Genetics and Biotechnology, College of Life Sciences, Kyung Hee University, 17104, Yongin-si, Gyeonggi-do, Korea.
Hyunjung ParkDepartment of Genetics and Biotechnology, College of Life Sciences, Kyung Hee University, 17104, Yongin-si, Gyeonggi-do, Korea.
Min Jee ChaeDepartment of Genetics and Biotechnology, College of Life Sciences, Kyung Hee University, 17104, Yongin-si, Gyeonggi-do, Korea.
Hye Jin ChoiDivision of Medical Oncology, Department of Internal Medicine, Yonsei University College of Medicine, 03722, Seoul, South Korea.
Do Young KimYonsei Liver Center, Severance Hospital, 03722, Seoul, South Korea. DYK1025@yuhs.ac.
Simon Weonsang RoDepartment of Genetics and Biotechnology, College of Life Sciences, Kyung Hee University, 17104, Yongin-si, Gyeonggi-do, Korea. simonro@khu.ac.kr.
Kyung Hee University · KRSeverance Hospital · KRYonsei University · KR

Funding

Kyung Hee University KHU-20201758National Research Foundation of Korea 2017R1C1B2007770National Research Foundation of Korea 2019R1A2C2009518National Research Foundation of Korea 2019R1I1A1A01055805
6 · The paper itself

Abstract

backgroundLiver cancer is a major global health concern due to the steady increases in its incidence and mortality. Transcription factors, yes-associated protein (YAP) and WW domain-containing transcription regulator protein 1 (WWTR1, also known as TAZ) have emerged as critical regulators in human hepatocellular carcinoma (HCC) and cholangiocarcinoma (CC), the two major types of primary liver cancer. However, our study as well as other previous reports have shown that activation of YAP and TAZ (YAP/TAZ) in adult murine livers is insufficient for the development of liver cancer, suggesting a requirement for an additional oncogenic collaborator for liver carcinogenesis in adulthood. Therefore, we sought to identify the oncogenic partners of YAP/TAZ that promote hepatocarcinogenesis in adults.

methodsData analysis of the transcriptome of patients with liver cancer was performed using the national center for biotechnology information (NCBI) gene expression omnibus (GEO) database and the cancer genome atlas (TCGA). The cancer therapeutics response portal (CTRP) was used to investigate the correlation between sensitivity to chemicals and the copy number of TAZ in human cancer cell lines. Transposons encoding constitutively activated forms of TAZ (TAZ

resultsThrough database analyses, we identified EGFR/HER2 signaling to be essential in human cancers with high TAZ activity. Furthermore, immunohistochemical analyses showed that human HCC and CC tissues with high YAP/TAZ activities exhibited concomitant activation of EGFR/HER2 signaling pathways. To demonstrate that EGFR/HER2 signaling promotes YAP/TAZ-mediated hepatocarcinogenesis, TAZ

conclusionsOur study demonstrates that TAZ collaborates with EGFR/HER2 signaling pathways to induce both HCC and CC.

Indexed as

Bile Duct NeoplasmsCarcinoma, HepatocellularCholangiocarcinomaLiver NeoplasmsAdultAnimalsBile Ducts, IntrahepaticCarcinogenesisErbB ReceptorsHumansMiceProto-Oncogene Proteins B-rafSignal TransductionTranscriptional Coactivator with PDZ-Binding Motif ProteinsEGFR protein, humanErbB ReceptorsProto-Oncogene Proteins B-rafTranscriptional Coactivator with PDZ-Binding Motif ProteinsWWTR1 protein, humanCholangiocarcinomaEGFR/HER2Hepatocellular carcinomaHydrodynamic transfectionTAZ

Identifiers

PMID35439973
PMCPMC9019950
OpenAlexW4226015339

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.