Malignant function of nuclear factor-kappaB axis in prostate cancer: Molecular interactions and regulation by non-coding RNAs

• Published in: Pharmacological research Vol. 194; p. 106775
• Main Authors: Al-Rashidi, Reyadh R., Noraldeen, Sara Abdalrazzaq M., Kareem, Ali Kamil, Mahmoud, Aisha Kamal, Kadhum, Wesam R., Ramírez-Coronel, Andrés Alexis, Iswanto, Acim Heri, Obaid, Rasha Fadhel, Jalil, Abduladheem Turki, Mustafa, Yasser Fakri, Nabavi, Noushin, Wang, Yuzhuo, Wang, Lin
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier Ltd 01.08.2023; Elsevier
• Subjects: Drug resistance; Inflammation; NF-κB axis; Prostate cancer; Urological cancers; NF-κB axis; Urological cancers; Inflammation; Drug resistance; Prostate cancer
• ISSN: 1043-6618; 1096-1186
• DOI: 10.1016/j.phrs.2023.106775

[Display omitted] Prostate carcinoma is a malignant situation that arises from genomic alterations in the prostate, leading to changes in tumorigenesis. The NF-κB pathway modulates various biological mechanisms, including inflammation and immune responses. Dysregulation of NF-κB promotes carcinogenesis, including increased proliferation, invasion, and therapy resistance. As an incurable disease globally, prostate cancer is a significant health concern, and research into genetic mutations and NF-κB function has the efficacy to facilitate the introduction of novel therapies. NF-κB upregulation is observed during prostate cancer progression, resulting in increased cell cycle progression and proliferation rates. Additionally, NF-κB endorses resistance to cell death and enhances the capacity for metastasis, particularly bone metastasis. Overexpression of NF-κB triggers chemoresistance and radio-resistance, and inhibition of NF-κB by anti-tumor compounds can reduce cancer progression. Interestingly, non-coding RNA transcripts can regulate NF-κB level and its nuclear transfer, offering a potential avenue for modulating prostate cancer progression.