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DAL-1 attenuates epithelial to mesenchymal transition and metastasis by suppressing HSPA5 expression in non-small cell lung cancer.
- Source :
-
Oncology reports [Oncol Rep] 2017 Nov; Vol. 38 (5), pp. 3103-3113. Date of Electronic Publication: 2017 Sep 26. - Publication Year :
- 2017
-
Abstract
- Metastasis is the primary cause of death in lung cancer patients and EMT (epithelial-mesenchymal transition) promotes metastasis. Previous study revealed that DAL-1 (differentially expressed in adenocarcinoma of the lung) could attenuate EMT and metastasis in non-small cell lung cancer (NSCLC). Further study proved that HSPA5 (heat shock protein 5), which has a promoting effect on EMT, could bind to DAL-1. In this study, the mRNA and protein expression levels of target molecules were detected by RTq-PCR and western blot assays, the migration and invasion abilities were examined by Transwell migration and invasion assay, and the proliferation ability was measured by CCK-8 assay. We revealed that DAL-1 was downregulated while HSPA5 was upregulated in NSCLC and found the protein of DAL-1 and HSPA5 co-localized in the cytoplasm and nucleus. We demonstrated that DAL-1 can suppress the expression of HSPA5 on mRNA and protein levels, and decrease EMT, migration, invasion and proliferation abilities by down-regulating HSPA5. Furthermore, we discovered that DAL-1 plays a role in inhibiting PI3K/Akt/Mdm2 signaling pathway by suppressing HSPA5.
- Subjects :
- A549 Cells
Carcinoma, Non-Small-Cell Lung pathology
Cell Movement genetics
Endoplasmic Reticulum Chaperone BiP
Epithelial-Mesenchymal Transition genetics
Gene Expression Regulation, Neoplastic
Humans
Neoplasm Invasiveness genetics
Neoplasm Invasiveness pathology
Phosphatidylinositol 3-Kinases genetics
RNA, Messenger
Signal Transduction genetics
Carcinoma, Non-Small-Cell Lung genetics
Cell Proliferation genetics
Heat-Shock Proteins genetics
Microfilament Proteins genetics
Subjects
Details
- Language :
- English
- ISSN :
- 1791-2431
- Volume :
- 38
- Issue :
- 5
- Database :
- MEDLINE
- Journal :
- Oncology reports
- Publication Type :
- Academic Journal
- Accession number :
- 29048640
- Full Text :
- https://doi.org/10.3892/or.2017.6000