ArticleScientific reports2018
Triciribine increases LDLR expression and LDL uptake through stabilization of LDLR mRNA.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 38 citations in OpenAlex.
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- Resveratrol improved atherosclerosis by increasing LDLR levels via the EGFR-ERK1/2 signaling pathway.Lipids in health and disease · 2025Article
- Interaction of AURKA with TRIM28 revives dormant LSCC cells via Akt signaling pathway to promote LSCC metastasis.Cancer cell international · 2025Article
- Autophagy regulates MK-2206-induced LDL receptor expression and cholesterol efflux pathways.PloS one · 2025Article
- Expanding drug targets for 112 chronic diseases using a machine learning-assisted genetic priority score.Nature communications · 2024Article
- The role of chromium supplementation in cardiovascular risk factors: A comprehensive reviews of putative molecular mechanisms.Heliyon · 2023Review
- Triciribine attenuates pathological neovascularization and vascular permeability in a mouse model of proliferative retinopathy.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2023Article
- High fat diet and PCSK9 knockout modulates lipid profile of the liver and changes the expression of lipid homeostasis related genes.Nutrition & metabolism · 2023Article
- Cold shock domain-containing protein E1 is a posttranscriptional regulator of the LDL receptor.Science translational medicine · 2022Article
- Regulation of low-density lipoprotein receptor expression in triple negative breast cancer by EGFR-MAPK signaling.Scientific reports · 2021Article
- Triciribine Engages ZFP36L1 and HuR to Stabilize LDLR mRNA.Molecules (Basel, Switzerland) · 2020Article
- The atheroprotective roles of heart-protecting musk pills against atherosclerosis development in apolipoprotein E-deficient mice.Annals of translational medicine · 2019Article
- Inhibitors of AKT kinase increase LDL receptor mRNA expression by two different mechanisms.PloS one · 2019Article
- Therapeutic targets of hypercholesterolemia: HMGCR and LDLR.Diabetes, metabolic syndrome and obesity : targets and therapy · 2019Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Low-density lipoprotein receptor (LDLR) is a key regulator of the metabolism of plasma low-density lipoprotein cholesterol (LDL-C), the elevated levels of which are associated with an increased risk of cardiovascular disease. Therefore, enhancing LDLR expression represents a potent treatment strategy for hypercholesterolemia. Here, we report that in cultured human hepatoma cells, triciribine, a highly selective AKT inhibitor, increases the stability of LDLR mRNA, an event that translates into upregulation of cell-surface LDLR levels and induction of cellular LDL uptake. This effect of triciribine requires ERK activity and is partially dependent on the intervening sequence between the AU-rich elements ARE3 and ARE4 in LDLR 3'UTR. We also show that triciribine downregulates the expression of PCSK9 mRNA and blunts the secretion of its protein. Notably, triciribine was found to potentiate the effect of mevastatin on LDLR protein levels and activity. We also show that primary human hepatocytes respond to triciribine by increasing the expression of LDLR. Furthermore, a pilot experiment with mice revealed that a two-weeks treatment with triciribine significantly induced the hepatic expression of LDLR protein. These results identify triciribine as a novel LDLR-elevating agent and warrant further examination of its potential as a hypocholesterolemic drug either as monotherapy or in combination with statins.
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