---
title: "Na+/K+-ATPase Blockade with Digoxin Reduces Proliferation and Metabolism in K562 Leukemia Cells"
id: "biorxiv-0-na-k-atpase-blockade-reversibly-attenuates-proliferation-and-metabolic-function"
canonical_url: "https://medichelpline.com/clinical-feed/biorxiv-0-na-k-atpase-blockade-reversibly-attenuates-proliferation-and-metabolic-function"
content_type: "clinical_feed_article"
specialty: "Hematology"
source_name: "bioRxiv (Biomedical Preprints)"
source_url: "https://www.biorxiv.org/content/10.64898/2026.09.11.751086v1?rss=1"
published_at: "2026-09-17T12:00:00.000Z"
evidence_level: "Verified Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Na+/K+-ATPase Blockade with Digoxin Reduces Proliferation and Metabolism in K562 Leukemia Cells
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/biorxiv-0-na-k-atpase-blockade-reversibly-attenuates-proliferation-and-metabolic-function
- **Specialty:** [Hematology](https://medichelpline.com/clinical-feed/hematology.md)
- **Primary Source:** bioRxiv (Biomedical Preprints)
- **Source URL:** [Original Journal Publication](https://www.biorxiv.org/content/10.64898/2026.09.11.751086v1?rss=1)
- **Published At:** 2026-09-17T12:00:00.000Z
- **Evidence Rating:** Verified Feed
## Executive GIST (TL;DR)
- The study examined effects of pharmacological blockade of the **Na+/K+-ATPase** (NKA) using digoxin in K562 human chronic myelogenous leukemia cells. - Submicromolar digoxin exposure produced a concentration-dependent reduction in cell proliferation with an reported IC50 of **151.0 nM**. - Digoxin caused a statistically significant depression of metabolic reducing capacity while **cell viability was not impaired**, indicating a cytostatic rather than cytotoxic effect. - Supplementation with extracellular potassium salts shifted digoxin sensitivity to the right in a surmountable manner, supporting that growth inhibition arises from **on-target NKA pump occupancy** rather than nonspecific interactions. - The observed growth attenuation and metabolic depression were fully reversible after drug clearance, demonstrating phenotypic recovery upon removal of NKA blockade. - Because K562 cells carry constitutive BCR-ABL kinase activity and have non-functional TP53 plus a homozygous deletion of CDKN2A (p16INK4a), canonical checkpoint responses are largely inactive; authors infer that NKA perturbation reduces growth mainly via **ion dyshomeostasis** and impaired secondary active transport rather than scaffold-mediated signaling. - The authors propose a model using K562 cells to dissect how NKA activity influences cancer cell proliferation and ion-mediated changes in cellular physiology. - This work is a preprint and has not undergone peer review; funding was declared from the NIH Common Fund (P20GM103442).
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Simon R Bowden 1 University of Mary; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Simon%2BR%2BBowden%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Bowden%20SR&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3ASimon%2BR%2BBowden%2B) Eli T Colton 1 University of Mary; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Eli%2BT%2BColton%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Colton%20ET&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AEli%2BT%2BColton%2B) Amber D Norgaard 1 University of Mary; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Amber%2BD%2BNorgaard%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Norgaard%20AD&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AAmber%2BD%2BNorgaard%2B) McKenzie M Haas 1 University of Mary; 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* [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Joseph%2BPatrick%2BBiggane%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Biggane%20JP&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AJoseph%2BPatrick%2BBiggane%2B) * [ORCID record for Joseph Patrick Biggane](http://orcid.org/0000-0002-7857-2450 "Open in new tab") * For correspondence: jpbiggane@umary.edu * [Abstract](https://www.biorxiv.org/content/10.64898/2026.09.11.751086v1)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_art/node:5786330/1) * [Info/History](https://www.biorxiv.org/content/10.64898/2026.09.11.751086v1.article-info)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_info/node:5786330/1) * [Metrics](https://www.biorxiv.org/content/10.64898/2026.09.11.751086v1.article-metrics)[](https://www.biorxiv.org/panels_ajax_tab/article_tab_metrics/node:5786330/1) * [ Preview PDF](https://www.biorxiv.org/content/10.64898/2026.09.11.751086v1.full.pdf+html)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_pdf/node:5786330/1) ![Loading](https://www.biorxiv.org/sites/all/modules/contrib/panels_ajax_tab/images/loading.gif) ## Abstract The Na+/K+-ATPase consumes a substantial portion of cellular ATP to maintain essential electrochemical gradients, yet its role in regulating cancer cell proliferation and phenotypic plasticity remains complicated by its dual function as an ion transporter and a scaffolding receptor. Here, we investigate the physiological consequences of pharmacological NKA blockade using digoxin in K562 human chronic myelogenous leukemia cells. Submicromolar digoxin exposure induced a concentration-dependent attenuation of cell proliferation (IC50 = 151.0 nM) and a statistically significant depression of metabolic reducing capacity without impairing cell viability. Competitive supplementation with extracellular potassium salts produced a surmountable rightward shift in digoxin sensitivity, confirming that growth inhibition is driven by on-target NKA pump occupancy rather than non-specific interactions. Furthermore, this cytostatic growth attenuation and metabolic depression were found to be fully reversible upon drug clearance. K562 cells are largely refractory to canonical kinase-overdrive stress checkpoints as they harbor constitutive BCR-ABL tyrosine kinase activity alongside non-functional _TP53_ and a homozygous deletion of _CDKN2A_ (p16INK4a). Consequently, these findings suggest that NKA perturbation attenuates K562 growth primarily through ion dyshomeostasis and secondary active transport constraints rather than scaffold-mediated signaling. Overall, we present a novel model for elucidating the role of the NKA in cancer proliferation and dissecting the mechanistic underpinnings of ion-mediated alterations in cancer cell physiology. ### Competing Interest Statement The authors have declared no competing interest. ## Funder Information Declared NIH Common Fund, P20GM103442 Copyright The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a [CC-BY 4.0 International license](http://creativecommons.org/licenses/by/4
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