Abstract
Nucleus-accumbens-associated protein-1 (NAC1) is a cancer-related transcriptional factor encoded by the NACC1 gene, which is amplified and overexpressed in various human cancers and has been appreciated as one of the top potential cancer driver genes. NAC1 has therefore been explored as a potential therapeutic target for managing malignant tumors. Here, we show that NAC1 is a negative regulator of NF-κB signaling, and NAC1 depletion enhances the level of the nuclear NF-κB in human melanoma. Furthermore, the inhibition of NF-κB signaling significantly potentiates the antineoplastic activity of the NAC1 inhibition in both the cultured melanoma cells and xenograft tumors. This study identifies a novel NAC1-NF-κB signaling axis in melanoma, offering a promising new therapeutic option to treat melanoma.
Document Type
Article
Publication Date
8-2023
Digital Object Identifier (DOI)
https://doi.org/10.3390/biomedicines11082221
Funding Information
This research was funded by [National Institutes of Health] grant number [RO1CA266579] And [National Institutes of Health] grant number [R01CA221867].
Repository Citation
Gu, Lixiang; Ren, Xingcong; Ngule, Chrispus; Xiong, Xiaofang; Song, Jianxun; Li, Zhiguo; and Yang, Jin-Ming, "Co-Targeting Nucleus Accumbens Associate 1 and NF-κB Signaling Synergistically Inhibits Melanoma Growth" (2023). Markey Cancer Center Faculty Publications. 316.
https://uknowledge.uky.edu/markey_facpub/316
Notes/Citation Information
© 2023 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https:// creativecommons.org/licenses/by/ 4.0/).