DLX4 promotes the expression of PD-L1 through GATA1 in Gestational Trophoblastic Neoplasia.

Autor: Wei Y; Department of Obstetrics and Gynecology, The First Affiliated Hospital of University of Science & Technology of China, Hefei, Anhui, PR China., Zhu CC; Department of Obstetrics and Gynecology, The First Affiliated Hospital of University of Science & Technology of China, Hefei, Anhui, PR China., Xu J; Department of Obstetrics and Gynecology, The First Affiliated Hospital of University of Science & Technology of China, Hefei, Anhui, PR China., Hu W; Department of Obstetrics and Gynecology, The First Affiliated Hospital of University of Science & Technology of China, Hefei, Anhui, PR China., Zhu J; Department of Obstetrics and Gynecology, The First Affiliated Hospital of University of Science & Technology of China, Hefei, Anhui, PR China. Electronic address: zhuj2442@163.com.
Jazyk: angličtina
Zdroj: Tissue & cell [Tissue Cell] 2024 Nov 29; Vol. 93, pp. 102641. Date of Electronic Publication: 2024 Nov 29.
DOI: 10.1016/j.tice.2024.102641
Abstrakt: Gestational Trophoblastic Neoplasia (GTN) is a highly malignant tumor that originates from trophoblastic cells during embryonic development. In this study, we observed that DLX4, a member of the Distal-Less Homeobox (Dlx) gene family, was upregulated in GTN tissues and cell lines. Bioinformatic analysis showed that DLX4 was highly expressed in most cancers and had a poor survival prognosis in certain tumors; further analysis showed that DLX4 was significantly associated with genes of immune pathways and immune infiltration. Functional analyses revealed that DLX4 overexpression or knockdown did not affect GTN cell proliferation; however, we observed that DLX4 could regulate PD-L1 expression via GATA1. The luciferase reporter activity of the wild-type construct increased after overexpression of GATA1, whereas the mutation of the binding sites abolished the transcriptional increase. In conclusion, our findings suggest that DLX4 regulates PD-L1 expression via GATA1 in GTN and may be a new target for antitumor therapy.
Competing Interests: Declaration of Competing Interest The authors declare no conflicts of interest.
(Copyright © 2024 The Authors. Published by Elsevier Ltd.. All rights reserved.)
Databáze: MEDLINE
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