Evidence map›Paper›PMID 33519235›Full record

ArticleCancer management and research2021

Plakophilin-2 Promotes Lung Adenocarcinoma Development via Enhancing Focal Adhesion and Epithelial-Mesenchymal Transition.

Yang Wu, Lu Liu, Xiaoyu Shen, Wenjing Liu, Rui Ma

Abstract read
In one paragraph

Article in Cancer management and research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

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21citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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3 · Its place in the literature

Who cites it

21 citing papers in PubMed.

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  19. Desmosomes as Signaling Hubs in the Regulation of Cell Behavior.Frontiers in cell and developmental biology · 2021
    Review
  20. Genomics and Prognosis Analysis of NFrontiers in genetics · 2021
    Article
4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

5 authors.

Yang WuMedical Oncology Department of Thoracic Cancer (2), Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, Shenyang 110042, Liaoning, People's Republic of China.
Lu LiuInstitute of Cancer Stem Cell, Dalian Medical University, Dalian 116044, Liaoning, People's Republic of China.ORCID 0000-0002-6812-7951
Xiaoyu ShenMedical Oncology Department of Thoracic Cancer (2), Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, Shenyang 110042, Liaoning, People's Republic of China.
Wenjing LiuMedical Oncology Department of Thoracic Cancer (2), Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, Shenyang 110042, Liaoning, People's Republic of China.
Rui MaMedical Oncology Department of Thoracic Cancer (2), Cancer Hospital of China Medical University, Liaoning Cancer Hospital & Institute, Shenyang 110042, Liaoning, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLung cancer is one of the most aggressive tumors with high incidence and mortality, which could be classified into lung squamous cell carcinoma (LUSC) and lung adenocarcinoma (LUAD). Overexpression of Plakophilin-2 (PKP2) has been reported in multiple malignancies. However, the expression and function mechanism of PKP2 in LUAD remain illusive.

methodsReal-time PCR (RT-PCR) was conducted to assess the expression of PKP2 in LUAD cells and tissues. An integrated analysis of PKP2 expression in The Cancer Genome Atlas (TCGA) was further performed. The effect of PKP2 on cell proliferation and invasion potential were then evaluated with loss-of-function assays in vitro. Xenograft nude mouse models were used to determine the role of PKP2 in LUAD tumorigenicity in vivo. Bioinformatics prediction, immunohistochemistry and Western blot were performed to examine whether PKP2 promoted LUAD development via enhancing focal adhesion and epithelial-mesenchymal transition.

resultsPKP2 expression was highly expressed in LUAD tissues compared with that in normal tissues and predicated poor prognosis of LUAD patients. TCGA LUAD cohort analysis also showed that high expression of PKP2 indicated unfavorable outcomes in LUAD patients. PKP2 expression was also upregulated in lung cancer cells. Functionally, knockdown of PKP2 suppressed lung cancer cell proliferation and invasion in vitro, while inhibited xenograft lung tumor development in vivo. Mechanistically, we demonstrated that high expression of PKP2 in LUAD was correlated with enhanced EMT and focal adhesion. Knockdown of PKP2 inhibited the expression of EMT-related Vimentin and N-cadherin and focal adhesion-associated expression of BMP4, ICAM1, and VCAM1 in xenograft tumors and lung cancer cells.

conclusionIn summary, our findings indicate that PKP2 functions as an oncogene in LUAD, which could be utilized as a novel diagnostic and therapeutic marker for LUAD treatment.

Indexed as

EMTfocal adhesionlung adenocarcinomaPKP2

Identifiers

PMID33519235
PMCPMC7837596

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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.