@Article{or.2024.048054,
AUTHOR = {XIUWANG WEI, JIANBO LIANG, HUANWEN HUANG, DAMING YANG, XINXIN WANG, XIUJIA WANG, CHANGSHENG CHEN, KAIQIANG LI, TAISEN PANG, BIN HU, FENGNING WU},
TITLE = {TMED3 promotes prostate cancer via FOXO1a and FOXO3a phosphorylation},
JOURNAL = {Oncology Research},
VOLUME = {33},
YEAR = {2025},
NUMBER = {1},
PAGES = {161--169},
URL = {http://www.techscience.com/or/v33n1/59088},
ISSN = {1555-3906},
ABSTRACT = { <b>Background:</b> Transmembrane emp24 trafficking protein 3 (TMED3) is associated with the development of several tumors; however, whether TMED3 regulates the progression of prostate cancer remains unclear. <b>Materials and Methods:</b> Short hairpin RNA was performed to repress TMED3 in prostate cancer cells (DU145 cells) and in a prostate cancer mice model to determine its function in prostate cancer <i>in vitro</i> and <i>in vivo</i>. <b>Results:</b> In the present study, we found that TMED3 was highly expressed in prostate cancer cells. <i>In vitro</i>, shTMED3 treatment suppressed the proliferation, invasion, and migration and promoted the apoptosis of DU145 cells. Additionally, the Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis showed a strong correlation between TMED3 and forkhead box O transcription factor (FOXO) pathway. Furthermore, TMED3 inhibition efficiently decreased FOXO1a and FOXO3a phosphorylation. <i>In vivo</i>, TMED3 downregulation suppressed the apoptosis, growth, and metastasis of prostate cancer cells via FOXO1a and FOXO3a. <b>Conclusion:</b> The present findings show that TMED3 participates in the regulation of prostate cancer progression via FOXO1a and FOXO3a phosphorylation, thereby revealing a novel mechanism underlying prostate cancer development and suggesting that TMED3 inhibition may serve as a novel strategy for prostate cancer treatment.},
DOI = {10.32604/or.2024.048054}
}