4.4 Article

LMNB1 targets FOXD1 to promote progression of prostate cancer

Journal

EXPERIMENTAL AND THERAPEUTIC MEDICINE
Volume 26, Issue 5, Pages -

Publisher

SPANDIDOS PUBL LTD
DOI: 10.3892/etm.2023.12212

Keywords

forkhead box D1; lamin B1; prostate cancer; viability; apoptosis

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The expression of FOXD1 is upregulated in prostate cancer, and its high expression is associated with clinical stage and survival. It regulates the expression of LMNB1 to promote viability, migration, and invasion of prostate cancer cells.
Forkhead box D1 (FOXD1) expression is upregulated in various types of human cancer. To the best of our knowledge, the roles of FOXD1 in prostate cancer (PC) remain largely unknown. The Cancer Genome Atlas dataset was used for the bioinformatics analysis of FOXD1 in PC. FOXD1 expression levels in normal immortalized human prostate epithelial cells (RWPE-1) and prostate cancer cells were detected by reverse transcription-quantitative PCR. PC cell viability was detected using Cell Counting Kit-8 assay. Transwell assays were performed to assess the migration and invasion of PC cells. Luciferase reporter gene assay was used to validate the association between FOXD1 and lamin (LMN)B1. LMNB1 is an important part of the cytoskeleton, which serves an important role in the process of tumor occurrence and development, regulating apoptosis and DNA repair. FOXD1 expression was upregulated in PC tissues, with its high expression being associated with clinical stage and survival in PC. Knockdown of FOXD1 inhibited viability, migration and invasion of PC cells. FOXD1 positively regulated LMNB1 expression. The effect of FOXD1 knockdown on PC cells was reversed by LMNB1 overexpression. In conclusion, FOXD1, positively regulated by LMNB1, served as an oncogene in PC and may be a potential biomarker and treatment target for PC.

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