---
title: "Sotagliflozin Modulates DNMT1 and HDAC Expression Alongside Anticancer Effects in Breast and Lung"
id: "pubmed-42677956"
canonical_url: "https://medichelpline.com/clinical-feed/pubmed-42677956"
content_type: "clinical_feed_article"
specialty: "Oncology"
source_name: "PubMed / NCBI"
source_url: "https://pubmed.ncbi.nlm.nih.gov/42677956/"
doi: "10.1002/cbin.70201"
published_at: "2026-09-01T00:00:00.000Z"
evidence_level: "Journal Article"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Sotagliflozin Modulates DNMT1 and HDAC Expression Alongside Anticancer Effects in Breast and Lung
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/pubmed-42677956
- **Specialty:** [Oncology](https://medichelpline.com/clinical-feed/oncology.md)
- **Primary Source:** PubMed / NCBI
- **Source URL:** [Original Journal Publication](https://pubmed.ncbi.nlm.nih.gov/42677956/)
- **DOI:** [10.1002/cbin.70201](https://doi.org/10.1002%2Fcbin.70201)
- **Published At:** 2026-09-01T00:00:00.000Z
- **Evidence Rating:** Journal Article
## Executive GIST (TL;DR)
- The study examined anticancer effects of the dual SGLT1/2 inhibitor **sotagliflozin** in human breast (MCF-7) and lung (A549) cancer cell lines. - Sotagliflozin reduced **cell viability**, clonogenic survival, migration, and invasion in both cell models. - Treatment induced **G2/M cell-cycle arrest** and increased activation of **AMPK**, with alterations in **PTEN-AKT-mTOR** signalling. - Molecular docking predicted favourable interactions between sotagliflozin and DNA methyltransferases (DNMT1, DNMT3A, DNMT3B), with strongest predicted binding to **DNMT1** (binding energy reported as −8.9 kcal/mol in the source). - Experimental data showed reduced total DNMT enzymatic activity after sotagliflozin exposure, decreased DNMT1 mRNA and protein abundance, and lowered protein levels of class I and II histone deacetylases (HDAC1–4 and **HDAC6**). - Sotagliflozin was associated with autophagy-related changes, including accumulation of acidic vesicular organelles and increased abundance of autophagy markers LC3-II and Beclin-1. - Authors conclude sotagliflozin exerts broad anticancer effects in these cell lines and provide preliminary evidence linking treatment to modulation of **epigenetic regulators** (DNMT1 and HDACs), while noting that whether these epigenetic changes are causal or secondary to metabolic effects requires further investigation.
## Clinical Analysis & Structured Key Points
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Affiliations Expand ### Affiliation * 1 Department of Biochemistry and Molecular Biology, School of Biological Sciences, Central University of Kerala, Kasaragod, Kerala, India. * PMID: **42677956** * DOI: [ 10.1002/cbin.70201 ](https://doi.org/10.1002/cbin.70201) Item in Clipboard # Sotagliflozin, a Dual SGLT1/2 Inhibitor, Modulates DNMT1 and Class I/II HDAC Expression in Association With Anticancer Effects in Breast and Lung Cancer Cells P K Hima et al. Cell Biol Int. 2026 Sep. Show details Display options Display options Format Abstract PubMed PMID Cell Biol Int Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Cell+Biol+Int%22%5Bjour%5D&sort=date&sort_order=desc) * [ Search in NLM Catalog ](https://www.ncbi.nlm.nih.gov/nlmcatalog?term=%22Cell+Biol+Int%22%5BTitle+Abbreviation%5D) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42677956/) . 2026 Sep;50(9):e70201. doi: 10.1002/cbin.70201. ### Authors [P K Hima](https://pubmed.ncbi.nlm.nih.gov/?term=Hima+PK&cauthor_id=42677956)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42677956/#short-view-affiliation-1 "Department of Biochemistry and Molecular Biology, School of Biological Sciences, Central University of Kerala, Kasaragod, Kerala, India."), [K Aswathy](https://pubmed.ncbi.nlm.nih.gov/?term=Aswathy+K&cauthor_id=42677956)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42677956/#short-view-affiliation-1 "Department of Biochemistry and Molecular Biology, School of Biological Sciences, Central University of Kerala, Kasaragod, Kerala, India."), [Govinda Rao Duddukuri](https://pubmed.ncbi.nlm.nih.gov/?term=Duddukuri+GR&cauthor_id=42677956)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42677956/#short-view-affiliation-1 "Department of Biochemistry and Molecular Biology, School of Biological Sciences, Central University of Kerala, Kasaragod, Kerala, India.") ### Affiliation * 1 Department of Biochemistry and Molecular Biology, School of Biological Sciences, Central University of Kerala, Kasaragod, Kerala, India. * PMID: **42677956** * DOI: [ 10.1002/cbin.70201 ](https://doi.org/10.1002/cbin.70201) Item in Clipboard Cite Display options Display options Format Abstract PubMed PMID ## Abstract Sodium-glucose cotransporter (SGLT) inhibitors are increasingly recognised for anticancer activity beyond their established glycaemic effects. While selective SGLT2 inhibitors have been reported to suppress tumour cell proliferation and modulate AMPK/mTOR and PI3K/AKT signalling, whether dual SGLT1/2 inhibition is associated with modulation of epigenetic regulators has remained largely unexplored. Here, we investigated the anticancer effects of sotagliflozin, a dual SGLT1/2 inhibitor, in breast (MCF-7) and lung (A549) cancer cells. Sotagliflozin reduced cell viability, clonogenic survival, migration, and invasion, and these effects were accompanied by G2/M cell-cycle arrest, increased AMPK activation, and changes in PTEN-AKT-mTOR signalling. Molecular docking analysis predicted favourable interactions between sotagliflozin and DNA methyltransferases (DNMT1, DNMT3A, and DNMT3B), with the strongest predicted binding to DNMT1 (-8.9 kcal/mol). Consistent with these computational predictions, sotagliflozin treatment was associated with reduced total DNMT enzymatic activity, decreased DNMT1 mRNA and protein abundance, and reduced protein abundance of class I and class II histone deacetylases (HDAC1-4 and HDAC6) in both cell lines. In addition, sotagliflozin treatment was associated with autophagy-related changes, including increased acidic vesicular organelles together with elevated LC3-II and Beclin-1 protein abundance. Collectively, these findings demonstrate that sotagliflozin exerts broad anticancer effects in breast and lung cancer cells and provide preliminary evidence that its treatment is associated with modulation of DNMT1 and HDAC expression. Further studies are required to determine whether these epigenetic changes contribute directly to the observed cellular responses or represent downstream consequences of metabolic perturbation. **Keywords:** DNMT1; HDAC; SGLT1/2 inhibitor; anticancer activity; breast cancer; epigenetics; lung cancer; sotagliflozin. © 2026 International Federation for Cell Biology. [PubMed Disclaimer](https://pubmed.ncbi.nlm.nih.gov/disclaimer/) ## Similar articles * [ Luteoloside induces G0/G1 arrest and pro-death autophagy through the ROS-mediated AKT/mTOR/p70S6K signalling pathway in human non-small cell lung cancer cell lines. ](https://pubmed.ncbi.nlm.nih.gov/29024631/) Zhou M, Shen S, Zhao X, Gong X.Zhou M, et al.Biochem Biophys Res Commun. 2017 Dec 9;494(1-2):263-269. doi: 10.1016/j.bbrc.2017.10.042. Epub 2017 Oct 9.Biochem Biophys Res Commun. 2017.PMID: 29024631 * [ Selective inhibition of esophageal cancer cells by combination of HDAC inhibitors and Azacytidine. ](https://pubmed.ncbi.nlm.nih.gov/25923331/) Ahrens TD, Timme S, Hoeppner J, Ostendorp J, Hembach S, Follo M, Hopt UT, Werner M, Busch H, Boerries M, Lassmann S.Ahrens TD, et al.Epigenetics. 2015;10(5):431-45. doi: 10.1080/15592294.2015.1039216.Epigenetics. 2015.PMID: 25923331Free PMC article. * [ A new synthetic HDAC inhibitor, MHY218, induces apoptosis or autophagy-related cell death in tamoxifen-resistant MCF-7 breast cancer cells. ](https://pubmed.ncbi.nlm.nih.gov/21983700/) Park JH, Ahn MY, Kim TH, Yoon S, Kang KW, Lee J, Moon HR, Jung JH, Chung HY, Kim HS.Park JH, et al.Invest New Drugs. 2012 Oct;30(5):1887-98. doi: 10.1007/s10637-011-9752-z. Epub 2011 Oct 8.Invest New Drugs. 2012.PMID: 21983700 * [ Inhibition of histone deacetylases promotes ubiquitin-dependent proteasomal degradation of DNA methyltransferase 1 in human breast cancer cells. ](https://pubmed.ncbi.nlm.nih.gov/18505931/) Zhou Q, Agoston AT, Atadja P, Nelson WG, Davidson NE.Zhou Q, et al.Mol Cancer Res. 2008 May;6(5):873-83. doi: 10.1158/1541-7786.MCR-07-0330.Mol Cancer Res. 2008.PMID: 18505931Free PMC article. * [ Sotagliflozin: Two Birds with One Stone? ](https://pubmed.ncbi.nlm.nih.gov/40465110/) Requena-Ibáñez JA, Kindberg KM, Santos-Gallego CG, Zafar MU, Badimon JJ.Requena-Ibáñez JA, et al.Cardiovasc Drugs Ther. 2026 Apr;40(2):671-679. doi: 10.1007/s10557-025-07723-z. Epub 2025 Jun 4.Cardiovasc Drugs Ther. 2026.PMID: 40465110Review. [ See all similar articles ](https://pubmed.ncbi.nlm.nih.gov/?linkname=pubmed_pubmed&from_uid=42677956) ## References 1. 1. Abdel‐Rafei, M. K., N. M. Thabet, L. A. Rashed, and E. M. Moustafa. 2021. “Canagliflozin, a SGLT‐2 Inhibitor, Relieves ER Stress, Modulates Autophagy and Induces Apoptosis in Irradiated HepG2 Cells: Signal Transduction Between PI3K/AKT/GSK‐3β/mTOR and Wnt/β‐Catenin Pathways; In Vitro.” Journal of Cancer Research and Therapeutics 17, no. 6: 1404–1418. . 2. 1. Anastasio, C., I. Donisi, V. Del Vecchio, et al. 2024. “SGLT2 Inhibitor Promotes Mitochondrial Dysfunction and ER‐Phagy in Colorectal Cancer Cells.” Cellular & Molecular Biology Letters 29, no. 1: 80. . 3. 1. Augoff, K., A. Hryniewicz‐Jankowska, R. Tabola, and K. Stach. 2022. “MMP9: A Tough Target for Targeted Therapy for Cancer.” Cancers 14, no. 7: 1847. . 4. 1. Bardaweel, S., and A. Issa. 2022. “Exploring the Role of Sodium–Glucose Cotransporter as a New Target for Cancer Therapy.” Journal of Pharmacy & Pharmaceutical Sciences: A Publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques 25: 253–265. . 5. 1. Basak, D., D. Gamez, and S. Deb. 2023. “SGLT2 Inhibitors as Potential Anticancer Agents.” Biomedicines 11, no. 7: 1867. . Show all 72 references ## MeSH terms * A549 Cells Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22A549+Cells%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=A549+Cells) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42677956/) * Antineoplastic Agents* / pharmacology Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Antineoplastic+Agents%2Fpharmacology%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Antineoplastic+Agents) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42677956/) * Breast Neoplasms* / drug therapy Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Breast+Neoplasms%2Fdrug+therapy%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Breast+Neoplasms) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42677956/) * Breast Neoplasms* / metabolism Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Breast+Neoplasms%2Fmetabolism%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Breast+Neoplasms) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42677956/) * Breast Neoplasms* / pathology Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Breast+Neoplasms%2Fpathology%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Breast+Neoplasms) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42677956/) * Cell Line, Tumor Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Cell+Line%2C+Tumor%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Cell+Line%2C+Tumor) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42677956/) * Cell Movement / drug effects Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Cell+Movement%2Fdrug+effects%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Cell+Movement) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42677956/) * Cell Proliferation / drug effects Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Cell+Proliferation%2Fdrug+effects%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Cell+Proliferation) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42677956/) * Cell Survival / drug effects Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Cell+Survival%2Fdrug+effects%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Cell+Survival) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42677956/) * DNA (Cytosine-5-)-Methyltransferase 1* / metabolism Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22DNA+%28Cytosine-5-%29-Methyltransferase+1%2Fmetabolism%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=DNA+%28Cytosine-5-%29-Methyltransferase+1) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42677956/) * DNA (Cytosine-5-)-Methyltransferases / metabolism Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22DNA+%28Cytosine-5-%29-Methyltransferases%2Fmetabolism%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=DNA+%28Cytosine-5-%29-Methyltransferases) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42677956/) * Female Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Female%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Female) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42677956/) * Glycosides* / pharmacology Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Glycosides%2Fpharmacology%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Glycosides) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42677956/) * Histone Deacetylase 2 / metabolism Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Histone+Deacetylase+2%2Fmetabolism%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Histone+Deacetylase+2) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42677956/) * Histone Deacetylases* / metabolism Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Histone+Deacetylases%2Fmetabolism%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Histone+Deacetylases) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42677956/) * Humans Ac
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