---
title: "MCT4/SLC16A3 Drives Myeloid Lactate Export in HNSCC Progression"
id: "biorxiv-0-mct4-associated-lactate-export-defines-myeloid-metabolic-reprogramming-during"
canonical_url: "https://medichelpline.com/clinical-feed/biorxiv-0-mct4-associated-lactate-export-defines-myeloid-metabolic-reprogramming-during"
content_type: "clinical_feed_article"
specialty: "Oncology"
source_name: "bioRxiv (Biomedical Preprints)"
source_url: "https://www.biorxiv.org/content/10.64898/2026.10.13.758108v1?rss=1"
published_at: "2026-10-16T09:06:41.000Z"
evidence_level: "Verified Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# MCT4/SLC16A3 Drives Myeloid Lactate Export in HNSCC Progression
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/biorxiv-0-mct4-associated-lactate-export-defines-myeloid-metabolic-reprogramming-during
- **Specialty:** [Oncology](https://medichelpline.com/clinical-feed/oncology.md)
- **Primary Source:** bioRxiv (Biomedical Preprints)
- **Source URL:** [Original Journal Publication](https://www.biorxiv.org/content/10.64898/2026.10.13.758108v1?rss=1)
- **Published At:** 2026-10-16T09:06:41.000Z
- **Evidence Rating:** Verified Feed
## Executive GIST (TL;DR)
- Investigators integrated single-cell RNA-sequencing (scRNA-seq) from five head and neck squamous cell carcinoma (**HNSCC**) cohorts totaling 645,351 cells from 114 patients to examine metabolic programs across cell populations. - The team applied single-cell Flux Estimation Analysis (scFEA) to infer metabolic flux allocation at single-cell resolution; the source reported use of scFEA but did not provide algorithmic parameters in the abstract. - Myeloid cells demonstrated the highest and most consistent allocation of inferred metabolic flux to **lactate** export among major tumor microenvironment cell types. - In a subset of ten patients with paired normal mucosa and carcinoma samples, myeloid lactate-export allocation rose from 1.72% to 3.31% of total inferred metabolic flux; every paired case showed an increase. - Within carcinoma samples, **SPP1+ macrophages** had the highest inferred lactate-export allocation of myeloid subtypes. - Lactate export correlated predominantly with **MCT4/SLC16A3** expression; in carcinoma myeloid cells, **SLC16A3** expression exceeded **SLC16A1** by 17-fold according to the source. - Independent protein-level data from CPTAC-HNSCC confirmed tumor enrichment of **MCT4** protein as reported in the article. - The authors framed increased **MCT4**-associated lactate export as a defining feature of myeloid metabolic reprogramming during HNSCC progression. - The article is a preprint and has not been peer reviewed; the abstract did not report experimental details such as scFEA parameter settings, normalization methods, or full cohort clinical annotations. - Data links and accession numbers were provided in footnotes (multiple GEO/GSA entries); funding sources included several NIH grants and institutional support.
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Thomas Tilton 1 University of Southern California; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Thomas%2BTilton%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Tilton%20T&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AThomas%2BTilton%2B) * [ORCID record for Thomas Tilton](http://orcid.org/0009-0002-2535-7973 "Open in new tab") Young Min Park 1 University of Southern California; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Young%2BMin%2BPark%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Park%20YM&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AYoung%2BMin%2BPark%2B) * [ORCID record for Young Min Park](http://orcid.org/0000-0002-7593-8461 "Open in new tab") Haiqi Zhu 2 Indiana University; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Haiqi%2BZhu%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Zhu%20H&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AHaiqi%2BZhu%2B) Chi Zhang 3 Oregon Health & Science University * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Chi%2BZhang%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Zhang%20C&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AChi%2BZhang%2B) * [ORCID record for Chi Zhang](http://orcid.org/0000-0001-9553-0925 "Open in new tab") De-Chen Lin 1 University of Southern California; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=De-Chen%2BLin%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Lin%20D&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3ADe-Chen%2BLin%2B) * [ORCID record for De-Chen Lin](http://orcid.org/0000-0002-1951-367X "Open in new tab") * For correspondence: dechenli@usc.edu * [Abstract](https://www.biorxiv.org/content/10.64898/2026.10.13.758108v1)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_art/node:5873471/1) * [Info/History](https://www.biorxiv.org/content/10.64898/2026.10.13.758108v1.article-info)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_info/node:5873471/1) * [Metrics](https://www.biorxiv.org/content/10.64898/2026.10.13.758108v1.article-metrics)[](https://www.biorxiv.org/panels_ajax_tab/article_tab_metrics/node:5873471/1) * [Supplementary material](https://www.biorxiv.org/content/10.64898/2026.10.13.758108v1.supplementary-material)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_data/node:5873471/1) * [Data/Code](https://www.biorxiv.org/content/10.64898/2026.10.13.758108v1.external-links)[](https://www.biorxiv.org/panels_ajax_tab/article_tab_data_code/node:5873471/1) * [ Preview PDF](https://www.biorxiv.org/content/10.64898/2026.10.13.758108v1.full.pdf+html)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_pdf/node:5873471/1) ![Loading](https://www.biorxiv.org/sites/all/modules/contrib/panels_ajax_tab/images/loading.gif) ## Abstract Head and neck squamous cell carcinoma (HNSCC) develops within a metabolically remodeled tumor microenvironment, yet how metabolic programs evolve across specific cell populations during tumor progression remains poorly understood. We integrated single-cell RNA-sequencing data from five HNSCC cohorts comprising 645,351 cells from 114 patients and inferred metabolic flux using single-cell Flux Estimation Analysis (scFEA). Myeloid cells showed the highest and most consistent metabolic allocation to lactate export among major cell types. In ten patients with paired normal mucosa and carcinoma, myeloid lactate-export allocation increased from 1.72% to 3.31% of total inferred metabolic flux, with an increase in every patient. SPP1+ macrophages showed the highest lactate-export allocation in carcinoma. Lactate export was predominantly associated with MCT4/SLC16A3. In carcinoma, myeloid SLC16A3 expression exceeded SLC16A1 by 17-fold, and CPTAC-HNSCC confirmed tumor enrichment of MCT4 protein. Together, these findings identify increased MCT4-associated lactate export as a prominent feature of myeloid metabolic reprogramming during HNSCC progression. ### Competing Interest Statement The authors have declared no competing interest. ## Footnotes * * * * * * ## Funder Information Declared National Cancer Institute, https://ror.org/040gcmg81, R37CA237022 National Institute of Dental and Craniofacial Research, https://ror.org/004a2wv92, R01DE033648 National Institute of Diabetes and Digestive and Kidney Diseases, https://ror.org/00adh9b73, R01DK135562 National Institute of Dental and Craniofacial Research, https://ror.org/004a2wv92, R01DE035339 Kure It Cancer Research University of Southern California 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/4.0/). bioRxiv and medRxiv thank the following for their generous financial support: > The Chan Zuckerberg Initiative, Cold Spring Harbor Laboratory, the Sergey Brin Family Foundation, California Institute of Technology, Centre National de la Recherche Scientifique, Fred Hutchinson Cancer Center, Imperial College London, Massachusetts Institute of Technology, Stanford University, The University of Edinburgh, University of Washington, and Vrije Universiteit Amsterdam. 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