Anti-PTK7 Monoclonal Antibodies Suppresses Oncogenic Phenotypes in Cellular and Xenograft Models of Triple-Negative Breast Cancer

Sep 23, 2026

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Protein tyrosine kinase 7 (PTK7) is frequently upregulated in cancers, including triple-negative breast cancer (TNBC), and its elevated expression links to poor clinical outcomes. TCGA analyses show higher PTK7 mRNA in TNBC tumors versus adjacent normal and other breast cancer subtypes, and Kaplan–Meier results associate high PTK7 with worse relapse-free survival. Anti-PTK7 monoclonal antibodies inhibit proliferation, wound healing, migration, and invasion in TNBC MDA-MB-231 cells, reduce Ki-67 signals, impair actin polymerization, and suppress tumor growth in xenografts.

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CategoryHealthcare

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Abstract

Introduction

Article Anti-PTK7 Monoclonal Antibodies Suppresses Oncogenic Phenotypes in Cellular and Xenograft Models of Triple-Negative Breast Cancer Min Ho Kim 1,†, Mi Kyung Park 2,3,†, Han Na Park 1, Seung Min Ham 1, Ho Lee 2, *,‡ and Seung-Taek Lee 1, *,‡ Academic Editor: Zhixiang Wang Received: 24 December 2024 Revised: 15 January 2025 Accepted: 21 January 2025 Published: 24 January 2025 Citation: Kim, M.H.; Park, M.K.; Park, H.N.; Ham, S.M.; Lee, H.; Lee, S.-T. Anti-PTK7 Monoclonal Antibodies Suppresses Oncogenic Phenotypes in Cellular and Xenograft Models of Triple-Negative Breast Cancer. Cells 2025, 14, 181. [https://](https://)[ ](https://)[doi.org/10.3390/cells14030181](doi.org/10.3390/cells14030181) [Copyright:](Copyright:) © 2025 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ([https://creativecommons.org/](https://creativecommons.org/)[ ](https://creativecommons.org/)[licenses/by/4.0/](licenses/by/4.0/)) . 1 Department of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul 03722, Republic of Korea; [tomorrow0918@naver.com](tomorrow0918@naver.com) (M.H.K.); [qkrgkssk1024@naver.com](qkrgkssk1024@naver.com) (H.N.P.); [mongsil1115@naver.com](mongsil1115@naver.com) (S.M.H.) 2 Department of Cancer Biomedical Science, Graduate School of Cancer Science and Policy, National Cancer Center, Goyang 10408, Republic of Korea; [mkpark@hsmu.ac.kr](mkpark@hsmu.ac.kr) 3 Department of Biomedical Science, Hwasung Medi-Science University, Hwaseong 18274, Republic of Korea * [Correspondence: ho25lee@ncc.re.kr](Correspondence: ho25lee@ncc.re.kr) (H.L.); [stlee@yonsei.ac.kr](stlee@yonsei.ac.kr) (S.-T.L.)† These authors contributed equally to this work. ‡ These authors contributed equally to this work. Abstract: Protein tyrosine kinase 7 (PTK7), a catalytically defective receptor protein tyrosine kinase, is frequently upregulated in various cancers, including triple-negative breast cancer (TNBC), and is associated with poor clinical outcomes. Analysis of The Cancer Genome Atlas (TCGA) data confirmed that PTK7 mRNA expression is significantly higher in TNBC tumor tissues compared with adjacent normal tissues and non-TNBC breast cancer subtypes. Kaplan–Meier survival analysis demonstrated a strong correlation between high PTK7 expression and worse relapse-free survival in TNBC patients (HR = 1.46, p = 0.015) . In vitro, anti-PTK7 monoclonal antibodies (mAbs) significantly reduced proliferation, wound healing, migration, and invasion in TNBC MDA-MB-231 cells. Ki-67 immunofluorescence assays revealed substantial decreases in cell proliferation following treatment with PTK7 mAbs (32-m, 43-m, 50-m, and 52-m) . Moreover, actin polymerization, a critical process in cell migration and invasion, was markedly impaired upon PTK7 mAb treatment. In vivo, PTK7 mAbs significantly reduced tumor volume and weight in a TNBC xenograft mouse model compared with controls. Treated tumors exhibited decreased expression of Ki-67 and vimentin, indicating reduced proliferation and epithelial-to-mesenchymal transition. These findings highlight PTK7 as a promising therapeutic target in TNBC and demonstrate the potent anti-cancer effects of PTK7-neutralizing mAbs both in vitro and in vivo. Further exploration of PTK7-targeted therapies, including humanized mAbs and antibody-drug conjugates, is warranted to advance treatment strategies for PTK7-positive TNBC. Keywords: MDA-MB-231 cells; monoclonal antibody; oncogene; PTK7; receptor protein tyrosine kinase; triple-negative breast cancer 1. Introduction Breast cancer (BC) is the most common cancer among women and a major cause of morbidity and mortality worldwide [1,2] . In the United States, in 2024, BC accounted for 32% of all cancers diagnosed in women and was the leading cause of cancer-related mortality among women aged 20 to 49

FAQs

What evidence links PTK7 expression to triple-negative breast cancer prognosis?

TCGA analysis shows PTK7 mRNA is higher in TNBC tumor tissues than in adjacent normal and other subtypes. Kaplan–Meier analysis links high PTK7 expression to worse relapse-free survival in TNBC patients.

How do anti-PTK7 monoclonal antibodies affect TNBC cells in vitro?

Anti-PTK7 monoclonal antibodies reduce proliferation and also suppress wound healing, migration, and invasion in MDA-MB-231 cells. Ki-67 immunofluorescence and actin polymerization assays show marked treatment-associated decreases.

What effects do anti-PTK7 antibodies produce in vivo using TNBC xenograft models?

In TNBC xenograft mice, PTK7 monoclonal antibodies significantly reduce tumor volume and weight versus controls. Treated tumors show decreased Ki-67 and vimentin expression, indicating reduced proliferation and epithelial-to-mesenchymal transition.

Sep 23, 2026

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