Open AccessCancer‐testis gene PIWIL 1 promotes cell proliferation, migration, and invasion in lung adenocarcinoma
Author(s) -
Xie Kaipeng,
Zhang Kai,
Kong Jing,
Wang Cheng,
Gu Yayun,
Liang Cheng,
Jiang Tingting,
Qin Na,
Liu Jibin,
Guo Xuejiang,
Huo Ran,
Liu Mingxi,
Ma Hongxia,
Dai Juncheng,
Hu Zhibin
Publication year - 2018
Publication title -
cancer medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 53
ISSN - 2045-7634
DOI - 10.1002/cam4.1248
Subject(s) - adenocarcinoma , biology , gene silencing , cancer research , lung cancer , dna methylation , gene , gene expression , cell growth , cancer , pathology , genetics , medicine
Piwi‐like RNA ‐mediated gene silencing 1 ( PIWIL 1 ) has been identified as a novel extremely highly expressed cancer‐testis ( CT ) gene in lung adenocarcinoma. However, the exact function and mechanism of PIWIL 1 in lung adenocarcinoma remains unclear. Herein, we sought to investigate the role of PIWIL 1 in the occurrence and development of lung adenocarcinoma. We examined the expression pattern of PIWIL 1 in The Cancer Genome Atlas ( TCGA ) lung adenocarcinoma samples, and validated it by Real‐Time PCR ( RT ‐ PCR ) in additional 21 paired lung adenocarcinoma tissues and 16 normal tissues. Subsequently, we explored the biological function of PIWIL 1 in A549 and H1299 cell lines by gain and loss‐of‐function analyses. Using TCGA lung adenocarcinoma data, we further performed coexpression and Gene Ontology ( GO ) analyses, and analyzed the association of DNA methylation levels in PIWIL 1 promoter region with its expression. Finally, we evaluated its expression in different mutation status of significantly mutated genes ( SMG s) in TCGA lung adenocarcinoma data. We observed that PIWIL 1 was expressed in testis and lung adenocarcinoma but not in other normal tissues, and its high expression was associated with shortened survival of lung cancer patients. Overexpression of PIWIL 1 could facilitate the proliferation, invasion and migration of lung adenocarcinoma cells and vice versa. GO analysis revealed that PIWIL 1 upregulated genes were enriched in embryonic development, cell proliferation and regulation of transcription. Moreover, promoter DNA hypomethylation of PIWIL 1 could contribute to its aberrant expression in tumors. Interestingly, PIWIL 1 expression was significantly higher in patients without hepatocyte growth factor ( HGF ) or serine/threonine kinase 11 ( STK 11 ) mutation ( P = 0.006 and 0.005, respectively). PIWIL 1 is an epidriver gene in lung adenocarcinoma, indicating a potential target for further therapy.