Cardamonin Counteracts Hypoxia-Induced Proliferation, Epithelial-Mesenchymal Transition (EMT) and Apoptosis Inhibition in Pancreatic Cancer Cells through Downregulating Aldo-Keto Reductase 1 Member B1 (AKR1B1)

Xiaojun Sun; Shanshan Sun

doi:10.23812/j.biol.regul.homeost.agents.20223604.118

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Asia Pacific Academy of Science Pte. Ltd. (APACSCI) specializes in international journal publishing. APACSCI adopts the open access publishing model and provides an important communication bridge for academic groups whose interest fields include engineering, technology, medicine, computer, mathematics, agriculture and forestry, and environment.

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Macrophages in the pathogenesis of psoriasis and anti-psoriatic nanotherapies

Psoriasis is a common, chronic, and inflammatory skin disease. Macrophages account for about 61.3% of the inflammatory cells infiltrating psoriatic lesions. Modulating macrophage polarization, inhibiting their infiltration, and targeting the secretion of inflammatory factors and associated inflammatory pathways by these cells can alleviate psoriasis symptoms and inflammation. Moreover, nanomaterials as novel drug carriers, offer unique advantages such as large surface area, easy modification, high biocompatibility, good biodegradability, enhanced systemic adsorption, etc. Nanomaterials have great potential for efficient drug delivery and release, as well as improving therapeutic efficacy while reducing adverse effects. By systematically addressing the role of macrophages in psoriasis pathogenesis and the potential of nanomaterials in treating psoriasis through modulating macrophages, this review enhances our understanding of the disease mechanism and holds promise for novel therapeutic breakthroughs and advancements in the future treatment of psoriasis.

Cardamonin Counteracts Hypoxia-Induced Proliferation, Epithelial-Mesenchymal Transition (EMT) and Apoptosis Inhibition in Pancreatic Cancer Cells through Downregulating Aldo-Keto Reductase 1 Member B1 (AKR1B1)

Xiaojun Sun, Shanshan Sun

Article ID: 6923
Vol 36, Issue 4, 2022

DOI: https://doi.org/10.23812/j.biol.regul.homeost.agents.20223604.118

Received: 8 September 2022; Accepted: 8 September 2022; Available online: 8 September 2022; Issue release: 8 September 2022

Abstract

Background: Pancreatic cancer (PC) is one of the deadliest malignancies, with poor prognosis. Hypoxia is commonly detected in pancreatic tumors and considered a stimulating factor for their progression. Studies have showed that Cardamonin (Cad) acts as a tumor suppressor in PC. This study explored the effect of Cad on PC progression under hypoxic conditions and the mechanism of this effect. Methods: Human PC cells (BxPC3 and PANC1) were treated with Cad, under hypoxic conditions. Pre-study bioinformatics analyses predicted that Cad targets aldo-keto reductase 1 member B1 (AKR1B1). The cytotoxicity of Cad at various concentrations on PC cells attacked by or not by hypoxic stress was determined with cell counting kit-8 assay. Cell invasion and apoptosis were measured with Transwell assay and flow cytometry, respectively. Expressions of N-Cadherin, E-Cadherin, matrix metalloproteinase (MMP)-9 and AKR1B1 in cells were analyzed with Western blot. Results: Cad delivered cytotoxicity to PC cells and the effect was dose dependent. Cad counteracted all the hypoxia-induced effects and downregulated AKR1B1. AKR1B1 overexpression potentiated these effects in hypoxia-induced PC cells and abrogated the Cad-induced countering effects. Conclusions: Cad downregulates AKR1B1 to counteract hypoxia-induced PC cell proliferation, epithelial-mesenchymal transition and apoptosis inhibition.

Keywords

cardamonin;hypoxia;apoptosis;epithelial-mesenchymal transition;aldo-keto reductase 1 member B1

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Medical Genetics, University of Torino Medical School, Italy

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2025-02-01

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