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ETS1 regulates NDRG1 to promote the proliferation, migration, and invasion of OSCC.
- Source :
-
Oral Diseases . Apr2024, Vol. 30 Issue 3, p977-990. 14p. - Publication Year :
- 2024
-
Abstract
- Objective: The aim of this study was to investigate the molecular mechanism by which the transcription factor ETS1 regulates N‐myc downstream regulatory gene 1 (NDRG1) to provide a new theoretical basis for the study of oral squamous cell carcinoma (OSCC). Methods: In this study, eight human OSCC and paraneoplastic samples were collected. The expressions of NDRG1, ETS1, and Ki67 were detected by immunohistochemistry; apoptosis was detected by tdt‐mediated dUTP notched end labeling; cell migration and invasion were detected by Transwell; quantitative real‐time PCR was performed to detect the expression of NDRG1; RNA‐binding protein immunoprecipitation (RIP) assays detected NDRG1 expression; immunofluorescence assays detected ETS1 expression. Results: NDRG1 and ETS1 expression was significantly upregulated in cancer tissues and CAL‐27 and SCC‐6 cells. Knockdown of NDRG1 and ETS1 inhibited cell proliferation, migration, invasion, cloning, and EMT while promoting apoptosis and inhibited tumor development; ETS1 positively regulated NDRG1 expression; Finally, overexpression of NDRG1 in vivo and in vitro reversed the effect of ETS1 knockdown on CAL‐27 and SCC‐6 cells. Conclusions: ETS1 positively regulates the expression of NDRG1 and promotes OSCC. Therefore, ETS1 may serve as a new target for the clinical diagnosis and treatment of OSCC. [ABSTRACT FROM AUTHOR]
- Subjects :
- *SQUAMOUS cell carcinoma
*IN vitro studies
*RNA-binding proteins
*CELL cycle proteins
*MOUTH tumors
*CANCER invasiveness
*RESEARCH funding
*CELL proliferation
*APOPTOSIS
*TRANSCRIPTION factors
*CELL motility
*QUANTITATIVE research
*REVERSE transcriptase polymerase chain reaction
*IN vivo studies
*MICE
*IMMUNOHISTOCHEMISTRY
*GENE expression
*ANIMAL experimentation
*PRECIPITIN tests
Subjects
Details
- Language :
- English
- ISSN :
- 1354523X
- Volume :
- 30
- Issue :
- 3
- Database :
- Academic Search Index
- Journal :
- Oral Diseases
- Publication Type :
- Academic Journal
- Accession number :
- 177191291
- Full Text :
- https://doi.org/10.1111/odi.14527