ArticleApplied biochemistry and biotechnology2026
Cancer Gene Therapy Utilizing NF-κB-regulated Expression of a miRNA Targeting RelA.
Article in Applied biochemistry and biotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundCancer continues to threat human health and life because of issues such as drug resistance and low response rates. The transcription factor NF-κB has emerged as a promising target for cancer therapy because of its overactivation in various cancers. However, existing NF-κB inhibitors lack cancer-cell specificity, leading to widespread suppression of essential physiological roles in immune regulation and cell survival, which results in systemic toxicity.
methodsIn contrast to the direct inhibition of NF-κB activity, this study introduces a novel antitumour strategy, DMP-miR533, which leverages NF-κB activity in cancer cells. This strategy employs a previously developed NF-κB-activated promoter, DMP, comprising five κB binding sites functioning as an NF-κB decoy and a minimal promoter, along with an artificial microRNA, miR533, that targets NF-κB RelA. Additionally, we constructed a variant with five copies of DMP-miR533, termed 5 × DMP-miR533.
resultsWe assessed the antitumour efficacy of DMP-miR533 in cultivated human and mouse cells and observed that both DMP-miR533 and 5 × DMP-miR533 induced significant cancer cell death, but didn’t affect the growth of normal cells. By encapsulating DMP-miR533 in an adeno-associated virus (AAV) vector to generate a recombinant AAV (rAAV), designated rAAV-DMP-miR533, significant inhibition of tumour growth was achieved through intravenous administration of rAAV in murine cancer models: H22 cell-formed hepatocellular carcinoma, WEHI-3 cell-formed leukaemia, and CT-26 cell-formed colon cancer. Notably, DMP-miR533 demonstrated substantial antitumour efficacy in both in vitro cell lines and in vivo mouse models without eliciting any observable side effects or toxicity.
conclusionThis study presents a promising and biosafe cancer gene therapy strategy involving regulation of NF-κB activity by a RELA-targeting microRNA, whose expression is controlled by a promoter that can sense the NF-κB activity in cells.
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