SDR42E1 modulates vitamin D absorption and cancer pathogenesis: insights from an in vitro model

IntroductionVitamin D is a pleiotropic hormone essential for bone health and overall physiological function. Despite its significance, vitamin D deficiency remains widespread and is often influenced by genetic factors. MethodsThis study investigates the role of SDR42E1, a gene encoding a short-chain...

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Main Authors: Nagham Nafiz Hendi, Georges Nemer
Format: Article
Language:English
Published: Frontiers Media S.A. 2025-07-01
Series:Frontiers in Endocrinology
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Online Access:https://www.frontiersin.org/articles/10.3389/fendo.2025.1585859/full
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author Nagham Nafiz Hendi
Nagham Nafiz Hendi
Georges Nemer
Georges Nemer
author_facet Nagham Nafiz Hendi
Nagham Nafiz Hendi
Georges Nemer
Georges Nemer
author_sort Nagham Nafiz Hendi
collection DOAJ
description IntroductionVitamin D is a pleiotropic hormone essential for bone health and overall physiological function. Despite its significance, vitamin D deficiency remains widespread and is often influenced by genetic factors. MethodsThis study investigates the role of SDR42E1, a gene encoding a short-chain dehydrogenase/reductase enzyme, in vitamin D regulation and sterol metabolism. Using CRISPR/Cas9 gene-editing, we generated an SDR42E1 knock-in model in HCT116 colorectal cells, which exhibit high endogenous SDR42E1 expression, harboring a nonsense variant associated with vitamin D deficiency.ResultsIntegrated transcriptomic and proteomic analyses revealed significant dysregulation of sterol absorption and metabolism (fold change (FC) = 1.8, P = 0.007) and cancer-related signaling pathways (FC = −1.7, P = 0.02). Notably, key differentially expressed genes included upregulated LRP1B and ABCC2, alongside downregulated WNT16 and SLC7A5. Proteomic profiling confirmed alterations in cell proliferation-related proteins, including reduced ALDOA expression (FC = −0.37, P = 0.0005). Functionally, SDR42E1 deficiency reduced cell viability by 53% (P = 0.0001), an effect reversed by transient SDR42E1 overexpression with restoring ABCC2 expression. ConclusionThese findings establish SDR42E1 as a key modulator of vitamin D-related pathways and highlight its potential as a therapeutic target for addressing vitamin D deficiency and associated pathologies, including cancer.
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spelling doaj-art-bc45fdf102e044aaa599a8887d466f6a2025-08-20T03:51:25ZengFrontiers Media S.A.Frontiers in Endocrinology1664-23922025-07-011610.3389/fendo.2025.15858591585859SDR42E1 modulates vitamin D absorption and cancer pathogenesis: insights from an in vitro modelNagham Nafiz Hendi0Nagham Nafiz Hendi1Georges Nemer2Georges Nemer3Faculty of Pharmacy, Middle East University, Amman, JordanDivision of Genomics and Translational Biomedicine, College of Health and Life Sciences, Hamad Bin Khalifa University, Doha, QatarDivision of Genomics and Translational Biomedicine, College of Health and Life Sciences, Hamad Bin Khalifa University, Doha, QatarDepartment of Biochemistry and Molecular Genetics, American University of Beirut, Beirut, LebanonIntroductionVitamin D is a pleiotropic hormone essential for bone health and overall physiological function. Despite its significance, vitamin D deficiency remains widespread and is often influenced by genetic factors. MethodsThis study investigates the role of SDR42E1, a gene encoding a short-chain dehydrogenase/reductase enzyme, in vitamin D regulation and sterol metabolism. Using CRISPR/Cas9 gene-editing, we generated an SDR42E1 knock-in model in HCT116 colorectal cells, which exhibit high endogenous SDR42E1 expression, harboring a nonsense variant associated with vitamin D deficiency.ResultsIntegrated transcriptomic and proteomic analyses revealed significant dysregulation of sterol absorption and metabolism (fold change (FC) = 1.8, P = 0.007) and cancer-related signaling pathways (FC = −1.7, P = 0.02). Notably, key differentially expressed genes included upregulated LRP1B and ABCC2, alongside downregulated WNT16 and SLC7A5. Proteomic profiling confirmed alterations in cell proliferation-related proteins, including reduced ALDOA expression (FC = −0.37, P = 0.0005). Functionally, SDR42E1 deficiency reduced cell viability by 53% (P = 0.0001), an effect reversed by transient SDR42E1 overexpression with restoring ABCC2 expression. ConclusionThese findings establish SDR42E1 as a key modulator of vitamin D-related pathways and highlight its potential as a therapeutic target for addressing vitamin D deficiency and associated pathologies, including cancer.https://www.frontiersin.org/articles/10.3389/fendo.2025.1585859/fullvitamin D regulationSDR42E1endocrine disordersgenetics in endocrinologyprecision medicine
spellingShingle Nagham Nafiz Hendi
Nagham Nafiz Hendi
Georges Nemer
Georges Nemer
SDR42E1 modulates vitamin D absorption and cancer pathogenesis: insights from an in vitro model
Frontiers in Endocrinology
vitamin D regulation
SDR42E1
endocrine disorders
genetics in endocrinology
precision medicine
title SDR42E1 modulates vitamin D absorption and cancer pathogenesis: insights from an in vitro model
title_full SDR42E1 modulates vitamin D absorption and cancer pathogenesis: insights from an in vitro model
title_fullStr SDR42E1 modulates vitamin D absorption and cancer pathogenesis: insights from an in vitro model
title_full_unstemmed SDR42E1 modulates vitamin D absorption and cancer pathogenesis: insights from an in vitro model
title_short SDR42E1 modulates vitamin D absorption and cancer pathogenesis: insights from an in vitro model
title_sort sdr42e1 modulates vitamin d absorption and cancer pathogenesis insights from an in vitro model
topic vitamin D regulation
SDR42E1
endocrine disorders
genetics in endocrinology
precision medicine
url https://www.frontiersin.org/articles/10.3389/fendo.2025.1585859/full
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