---
title: "KLF4-Driven KRT13+ Hillock-Like Cells in Lung Squamous Cell Carcinoma and Therapy Resistance"
id: "pubmed-42740576"
canonical_url: "https://medichelpline.com/clinical-feed/pubmed-42740576"
content_type: "clinical_feed_article"
specialty: "Oncology"
source_name: "PubMed / NCBI"
source_url: "https://pubmed.ncbi.nlm.nih.gov/42740576/"
doi: "10.1158/0008-5472.CAN-26-2945"
published_at: "2026-09-15T00:00:00.000Z"
evidence_level: "Journal Article"
license: "CC-BY-NC-4.0 / Informational Use"
---
# KLF4-Driven KRT13+ Hillock-Like Cells in Lung Squamous Cell Carcinoma and Therapy Resistance
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/pubmed-42740576
- **Specialty:** [Oncology](https://medichelpline.com/clinical-feed/oncology.md)
- **Primary Source:** PubMed / NCBI
- **Source URL:** [Original Journal Publication](https://pubmed.ncbi.nlm.nih.gov/42740576/)
- **DOI:** [10.1158/0008-5472.CAN-26-2945](https://doi.org/10.1158%2F0008-5472.CAN-26-2945)
- **Published At:** 2026-09-15T00:00:00.000Z
- **Evidence Rating:** Journal Article
## Executive GIST (TL;DR)
- Airway **hillocks** are specialized stratified squamous epithelial structures composed of luminal barrier cells supported by a basal stem cell population. - Izzo and colleagues identified a distinct population of slow-cycling **KRT13+** hillock-like tumor cells in **lung squamous cell carcinoma (SCC)**. - The **KRT13+** hillock-like cell state is conserved across multiple SCC models, indicating a recurrent tumor cell program. - Mechanistically, the transcription factor **KLF4** drives expression of **KRT13** in these cells. - KLF4-driven KRT13 expression in tumor cells correlates with enrichment of potential therapeutic targets and with resistance to **platinum-based chemotherapy**. - By linking a physiologic epithelial barrier cell program to treatment resistance, the study describes a previously uncharacterized mechanism important to SCC biology. - The findings were summarized in a Cancer Research comment by Xinyuan Tong and Hongbin Ji, which highlights the related original article by Izzo et al. (Cancer Res. 2026;86:4472–4496). - Publication identifiers noted in the source include PMID 42740576 and DOI 10.1158/0008-5472.CAN-26-2945. - Authors of the comment are affiliated with Shanghai Chest Hospital/Shanghai Jiao Tong University School of Medicine and Westlake University, indicating clinical and research context in thoracic oncology. - The comment frames the Izzo et al. work as connecting normal epithelial barrier biology to tumor cell states that may influence drug sensitivity and identify new therapeutic opportunities.
## Clinical Analysis & Structured Key Points
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Affiliations Expand ### Affiliations * 1 Shanghai Institute of Thoracic Oncology & Shanghai Key Laboratory of Thoracic Tumor Biotherapy, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. * 2 School of Medicine, Westlake University, Hangzhou, China. * PMID: **42740576** * DOI: [ 10.1158/0008-5472.CAN-26-2945 ](https://doi.org/10.1158/0008-5472.can-26-2945) Item in Clipboard Comment # A Barrier Betrayed: Hillock in Lung Squamous Cell Carcinoma Xinyuan Tong et al. Cancer Res. 2026. Show details Display options Display options Format Abstract PubMed PMID Cancer Res Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Cancer+Res%22%5Bjour%5D&sort=date&sort_order=desc) * [ Search in NLM Catalog ](https://www.ncbi.nlm.nih.gov/nlmcatalog?term=%22Cancer+Res%22%5BTitle+Abbreviation%5D) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42740576/) . 2026 Sep 15;86(18):4455-4456. doi: 10.1158/0008-5472.CAN-26-2945. ### Authors [Xinyuan Tong](https://pubmed.ncbi.nlm.nih.gov/?term=Tong+X&cauthor_id=42740576)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42740576/#short-view-affiliation-1 "Shanghai Institute of Thoracic Oncology & Shanghai Key Laboratory of Thoracic Tumor Biotherapy, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China."), [Hongbin Ji](https://pubmed.ncbi.nlm.nih.gov/?term=Ji+H&cauthor_id=42740576)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42740576/#short-view-affiliation-2 "School of Medicine, Westlake University, Hangzhou, China.") ### Affiliations * 1 Shanghai Institute of Thoracic Oncology & Shanghai Key Laboratory of Thoracic Tumor Biotherapy, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. * 2 School of Medicine, Westlake University, Hangzhou, China. * PMID: **42740576** * DOI: [ 10.1158/0008-5472.CAN-26-2945 ](https://doi.org/10.1158/0008-5472.can-26-2945) Item in Clipboard Cite Display options Display options Format Abstract PubMed PMID ## Abstract Airway hillocks are specialized, stratified squamous epithelial structures featuring luminal barrier cells supported by a dedicated basal stem cell population. In this issue of Cancer Research, Izzo and colleagues identify a distinct population of slow-cycling KRT13+ hillock-like tumor cells in lung squamous cell carcinoma, a cell state conserved across multiple squamous cell carcinoma (SCC) models. Mechanistically, KLF4 drives KRT13 expression, correlating with enrichment of potential therapeutic targets and resistance to platinum-based chemotherapy. By linking the physiologic epithelial barrier to therapeutic resistance, this study unlocks a previously uncharacterized mechanism underlying SCC biology. See related article by Izzo et al., p. 4472. ©2026 American Association for Cancer Research. [PubMed Disclaimer](https://pubmed.ncbi.nlm.nih.gov/disclaimer/) ## Comment on * [ KLF4 Promotes a KRT13+ Hillock-Like State in Lung Squamous Cell Carcinoma. ](https://pubmed.ncbi.nlm.nih.gov/42314152/) Izzo LT, Reyes T, Meesala S, Ireland AS, Earnest-Noble LB, Yang S, Sunil HS, Cheng XC, Tserentsoodol N, Hawgood SB, Glass C, Patz EF Jr, Witt BL, Tyson DR, O'Donnell KA, Oliver TG. Izzo LT, et al. Cancer Res. 2026 Sep 15;86(18):4472-4496. doi: 10.1158/0008-5472.CAN-26-0531. Cancer Res. 2026. PMID: 42314152 Free PMC article. ## Similar articles * [ KLF4 promotes a KRT13+ hillock-like state in squamous lung cancer. ](https://pubmed.ncbi.nlm.nih.gov/40161723/) Izzo LT, Reyes T, Meesala S, Ireland AS, Yang S, Sunil HS, Cheng XC, Tserentsoodol N, Hawgood SB, Patz EF Jr, Witt BL, Tyson DR, O'Donnell KA, Oliver TG.Izzo LT, et al.bioRxiv [Preprint]. 2025 Mar 13:2025.03.10.641898. doi: 10.1101/2025.03.10.641898.bioRxiv. 2025.Update in: [Cancer Res. 2026 Sep 15;86(18):4472-4496. doi: 10.1158/0008-5472.CAN-26-0531.](https://pubmed.ncbi.nlm.nih.gov/42314152/)PMID: 40161723Free PMC article.Updated.Preprint. * [ Krüppel-Like Factor 4 Enhances Sensitivity of Cisplatin to Esophageal Squamous Cell Carcinoma (ESCC) Cells. ](https://pubmed.ncbi.nlm.nih.gov/28694421/) Chen C, Ma Z, Zhang H, Liu X, Yu Z.Chen C, et al.Med Sci Monit. 2017 Jul 11;23:3353-3359. doi: 10.12659/msm.902583.Med Sci Monit. 2017.PMID: 28694421Free PMC article. * [ Persistent Krüppel-like factor 4 expression predicts progression and poor prognosis of head and neck squamous cell carcinoma. ](https://pubmed.ncbi.nlm.nih.gov/21219537/) Tai SK, Yang MH, Chang SY, Chang YC, Li WY, Tsai TL, Wang YF, Chu PY, Hsieh SL.Tai SK, et al.Cancer Sci. 2011 Apr;102(4):895-902. doi: 10.1111/j.1349-7006.2011.01859.x. Epub 2011 Mar 4.Cancer Sci. 2011.PMID: 21219537Free PMC article. * [ KLF4 suppresses the tumor activity of cutaneous squamous cell carcinoma (SCC) cells via the regulation of SMAD signaling and SOX2 expression. ](https://pubmed.ncbi.nlm.nih.gov/31284949/) Li XM, Kim SJ, Hong DK, Jung KE, Choi CW, Seo YJ, Lee JH, Lee Y, Kim CD.Li XM, et al.Biochem Biophys Res Commun. 2019 Sep 3;516(4):1110-1115. doi: 10.1016/j.bbrc.2019.07.011. Epub 2019 Jul 6.Biochem Biophys Res Commun. 2019.PMID: 31284949 * [ [Advances on driver oncogenes of squamous cell lung cancer]. ](https://pubmed.ncbi.nlm.nih.gov/24854563/) Hong W, Zhang Y.Hong W, et al.Zhongguo Fei Ai Za Zhi. 2014 May;17(5):433-6. doi: 10.3779/j.issn.1009-3419.2014.05.13.Zhongguo Fei Ai Za Zhi. 2014.PMID: 24854563Free PMC article.Review.Chinese. 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