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http://purl.uniprot.org/citations/36463587http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
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Background

Lung adenocarcinoma (LUAD) is one of the major subtypes of lung cancer and is the most common cause of cancer deaths globally. The Kank (kidney or KN motif and ankyrin repeat domain-containing) family of proteins has been characterized as critical for regulating the capacity of cells to migrate and their anti-tumor drug sensitivity. The current research designs to explore the specific effects and potential regulatory molecular mechanism of KANK3 on LUAD cells.

Method

Two datasets (TCGA-LUAD and GSE116959) were analyzed to confirm the differently expressed genes. qRT-PCR was carried out to measure KANK3 level in LUAD tissue samples and adjacent non-cancerous tissue samples. Western blot assay was utilized to investigate the KANK3, p-p38 and p38 protein levels. MTT assay were employed to investigate the cell proliferation. Cell invasion and migration were assessed using Transwell and wound healing assay.

Result

KANK3 was down-regulated in LUAD tissues and the expressions of KANK3 had a strong influence on prognosis of LUAD patients. Overexpression of KANK3 significantly inhibited， whereas KANK3 silencing observably enhanced the capacity of NCI-H1975 and PC-9 cells to proliferate, invade and migrate. GSEA showed that, differentially expressed genes which regulated by KANK3 enriched in cell adhesion, chemokine, focal adhesion or MAPK signaling pathway. Further experiments proved that KANK3 regulated LUAD cells proliferation and metastasis through p38 MAPK pathway.

Conclusion

KANK3 exerts antitumor effect in LUAD through regulation of p38 MAPK signaling pathway. These outcomes foreboded that KANK3 could be a novel therapeutic target for further study of LUAD."xsd:string
http://purl.uniprot.org/citations/36463587http://purl.org/dc/terms/identifier"doi:10.1016/j.tice.2022.101974"xsd:string
http://purl.uniprot.org/citations/36463587http://purl.uniprot.org/core/author"Chen X."xsd:string
http://purl.uniprot.org/citations/36463587http://purl.uniprot.org/core/author"Chen Q."xsd:string
http://purl.uniprot.org/citations/36463587http://purl.uniprot.org/core/author"Yang B."xsd:string
http://purl.uniprot.org/citations/36463587http://purl.uniprot.org/core/author"Hu C."xsd:string
http://purl.uniprot.org/citations/36463587http://purl.uniprot.org/core/author"Xie B."xsd:string
http://purl.uniprot.org/citations/36463587http://purl.uniprot.org/core/author"Dai Z."xsd:string
http://purl.uniprot.org/citations/36463587http://purl.uniprot.org/core/date"2023"xsd:gYear
http://purl.uniprot.org/citations/36463587http://purl.uniprot.org/core/name"Tissue Cell"xsd:string
http://purl.uniprot.org/citations/36463587http://purl.uniprot.org/core/pages"101974"xsd:string
http://purl.uniprot.org/citations/36463587http://purl.uniprot.org/core/title"KANK3 mediates the p38 MAPK pathway to regulate the proliferation and invasion of lung adenocarcinoma cells."xsd:string
http://purl.uniprot.org/citations/36463587http://purl.uniprot.org/core/volume"80"xsd:string
http://purl.uniprot.org/citations/36463587http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/36463587
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