GRPR Drives Metastasis via CRABP2 and FNDC4 Pathways in Lung Adenocarcinoma
Metastasis is a leading cause of lung adenocarcinoma (LUAD)-related mortality and presents significant challenges for treatment. The gastrin-releasing peptide receptor (GRPR), a member of the G protein-coupled receptor (GPCR) family, has an unclear role in LUAD progression. This study aimed to inves...
Saved in:
| Main Authors: | , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
MDPI AG
2024-12-01
|
| Series: | Cells |
| Subjects: | |
| Online Access: | https://www.mdpi.com/2073-4409/13/24/2128 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1850240956717072384 |
|---|---|
| author | Dong-Gun Kim Eun-Young Choi Hye-Mi Ahn Youn-Jae Kim |
| author_facet | Dong-Gun Kim Eun-Young Choi Hye-Mi Ahn Youn-Jae Kim |
| author_sort | Dong-Gun Kim |
| collection | DOAJ |
| description | Metastasis is a leading cause of lung adenocarcinoma (LUAD)-related mortality and presents significant challenges for treatment. The gastrin-releasing peptide receptor (GRPR), a member of the G protein-coupled receptor (GPCR) family, has an unclear role in LUAD progression. This study aimed to investigate the function and underlying mechanisms of GRPR in LUAD metastasis. Our findings revealed that GRPR levels were significantly elevated in tumor tissues, and higher <i>GRPR</i> expression was associated with worse overall survival outcomes. Functional assays demonstrated that <i>GRPR</i> overexpression enhanced LUAD cell invasion, while <i>GRPR</i> knockdown inhibited invasion both in vitro and in vivo. RNA sequencing and gene set enrichment analysis (GSEA) identified an enrichment of metastasis-promoting genes in <i>GRPR</i>-overexpressing cells, with CRABP2 and FNDC4 emerging as key targets. Clinical analyses further confirmed a positive correlation between <i>GRPR</i> expression and the levels of <i>CRABP2</i> and <i>FNDC4</i> in LUAD patients. These results suggest that GRPR could serve as both a prognostic marker and a therapeutic target to inhibit metastasis in LUAD. |
| format | Article |
| id | doaj-art-c3b64259d44845edb877b935861ab2e4 |
| institution | OA Journals |
| issn | 2073-4409 |
| language | English |
| publishDate | 2024-12-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Cells |
| spelling | doaj-art-c3b64259d44845edb877b935861ab2e42025-08-20T02:00:43ZengMDPI AGCells2073-44092024-12-011324212810.3390/cells13242128GRPR Drives Metastasis via CRABP2 and FNDC4 Pathways in Lung AdenocarcinomaDong-Gun Kim0Eun-Young Choi1Hye-Mi Ahn2Youn-Jae Kim3Targeted Therapy Branch, Division of Rare and Refractory Cancer, Research Institute, National Cancer Center, Goyang 10408, Republic of KoreaTargeted Therapy Branch, Division of Rare and Refractory Cancer, Research Institute, National Cancer Center, Goyang 10408, Republic of KoreaTargeted Therapy Branch, Division of Rare and Refractory Cancer, Research Institute, National Cancer Center, Goyang 10408, Republic of KoreaTargeted Therapy Branch, Division of Rare and Refractory Cancer, Research Institute, National Cancer Center, Goyang 10408, Republic of KoreaMetastasis is a leading cause of lung adenocarcinoma (LUAD)-related mortality and presents significant challenges for treatment. The gastrin-releasing peptide receptor (GRPR), a member of the G protein-coupled receptor (GPCR) family, has an unclear role in LUAD progression. This study aimed to investigate the function and underlying mechanisms of GRPR in LUAD metastasis. Our findings revealed that GRPR levels were significantly elevated in tumor tissues, and higher <i>GRPR</i> expression was associated with worse overall survival outcomes. Functional assays demonstrated that <i>GRPR</i> overexpression enhanced LUAD cell invasion, while <i>GRPR</i> knockdown inhibited invasion both in vitro and in vivo. RNA sequencing and gene set enrichment analysis (GSEA) identified an enrichment of metastasis-promoting genes in <i>GRPR</i>-overexpressing cells, with CRABP2 and FNDC4 emerging as key targets. Clinical analyses further confirmed a positive correlation between <i>GRPR</i> expression and the levels of <i>CRABP2</i> and <i>FNDC4</i> in LUAD patients. These results suggest that GRPR could serve as both a prognostic marker and a therapeutic target to inhibit metastasis in LUAD.https://www.mdpi.com/2073-4409/13/24/2128lung adenocarcinomametastasisGRPRAKTCRAPB2FNCD4 |
| spellingShingle | Dong-Gun Kim Eun-Young Choi Hye-Mi Ahn Youn-Jae Kim GRPR Drives Metastasis via CRABP2 and FNDC4 Pathways in Lung Adenocarcinoma Cells lung adenocarcinoma metastasis GRPR AKT CRAPB2 FNCD4 |
| title | GRPR Drives Metastasis via CRABP2 and FNDC4 Pathways in Lung Adenocarcinoma |
| title_full | GRPR Drives Metastasis via CRABP2 and FNDC4 Pathways in Lung Adenocarcinoma |
| title_fullStr | GRPR Drives Metastasis via CRABP2 and FNDC4 Pathways in Lung Adenocarcinoma |
| title_full_unstemmed | GRPR Drives Metastasis via CRABP2 and FNDC4 Pathways in Lung Adenocarcinoma |
| title_short | GRPR Drives Metastasis via CRABP2 and FNDC4 Pathways in Lung Adenocarcinoma |
| title_sort | grpr drives metastasis via crabp2 and fndc4 pathways in lung adenocarcinoma |
| topic | lung adenocarcinoma metastasis GRPR AKT CRAPB2 FNCD4 |
| url | https://www.mdpi.com/2073-4409/13/24/2128 |
| work_keys_str_mv | AT donggunkim grprdrivesmetastasisviacrabp2andfndc4pathwaysinlungadenocarcinoma AT eunyoungchoi grprdrivesmetastasisviacrabp2andfndc4pathwaysinlungadenocarcinoma AT hyemiahn grprdrivesmetastasisviacrabp2andfndc4pathwaysinlungadenocarcinoma AT younjaekim grprdrivesmetastasisviacrabp2andfndc4pathwaysinlungadenocarcinoma |