Integrins linked kinase and focal adhesion kinase as the key signaling mediators of vascular mimicry in metastatic breast tumor cells

Sep 21, 2026

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Breast cancer metastasis relies on vasculogenic mimicry (VM), where aggressive tumor cells form vascular-like channels that support invasion and delivery of blood to tumors. This research note investigates how focal adhesion kinase (FAK) and integrins linked kinase (ILK) contribute to VM progression in metastatic breast tumor cells. Metastatic cells from mice were analyzed in vitro and by real-time PCR, and ILK/FAK levels were found significantly elevated in highly metastatic lines.

LanguageEnglish

CategoryHealthcare

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Kamalabadi-Farahani et al. BMC Research Notes (2024) 17:282 BMC Research Notes [https://doi.org/10.1186/s13104-024-06953-y](https://doi.org/10.1186/s13104-024-06953-y) RESEARCH NOTE Open Access Integrins linked kinase and focal adhesion kinase as the key signaling mediators of vascular mimicry in metastatic breast tumor cells Mohammad Kamalabadi-Farahani 1, Vahid Kia2*, Sadegh Dylami3 and Amir Atashi4 Abstract Objective In highly aggressive malignant cancers including breast cancer, vasculogenic mimicry (VM) is the potential of tumor cells to generate a vascular channel network for delivering blood to tumor cells. Detection of genes involved in this process is critical to designing targeted therapy against breast cancer metastasis. In this study, we evaluated the roles of FAK and ILK in the progression of VM in metastatic breast tumor cells. Results Primary (4T1T), and highly metastatic (4T1B and 4T1L) breast tumor cells were isolated from cancerous mice. The potential of cancer cells to organize themselves into vascular-like structures (VM) has been evaluated with in vitro assessment. The expression of ILK and FAK were examined using real-time polymerase chain reaction. We confirmed the high ability of metastatic tumor cells in vascular-like structure formation. In molecular analysis, our data showed that ILK and FAK expression was significantly elevated in metastatic breast tumor cells. These results indicated that the higher potential of metastatic tumor cells in vascular-like structure formation may be related to higher expression of ILK and FAK. Analysis of molecular features of metastatic tumor cells could be utilized to create a targeted therapeutic strategy against metastasis in breast cancer. Keywords Breast cancer, Metastasis, Vascular mimicry, Integrins linked kinase (ILK), Focal adhesion kinase (FAK) *Correspondence: Vahid Kia [vahidkiaa@gmail.com](vahidkiaa@gmail.com) 1Department of Tissue Engineering, School of Medicine, Shahroud University of Medical Sciences, Shahroud, Iran 2Department of Medical Biotechnology, School of Medicine, Shahroud University of Medical Sciences, Shahroud, Iran 3Student Research Committee, School of Medicine, Shahroud University of Medical Sciences, Shahroud, Iran 4Department of Medical Laboratory Sciences, School of Allied Medical Sciences, Shahroud University of Medical Sciences, Shahroud, Iran Introduction Breast cancer metastasis results in 90% of mortality from breast cancer in women worldwide [1]. Identification mechanism that can promote metastasis, invasion and cell migration is vital to designing targeted therapy against breast cancer [2]. One of the main mechanism that can facilitate metastasis and tumorigenesis in breast cancer is vascular mimicry (VM) [3]. VM is formation a tubular structure independent of endothelial cells in tumor cells for enhancing survival and metastasis [4]. VM is triggered through a wide range of genes with performance associated to tumor invasion, metastasis, hypoxia and angiogenesis [5]. Contribution © The Author(s) 2024. Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly

FAQs

What is vasculogenic mimicry (VM) in metastatic breast cancer?

VM is the formation of tubular, vascular-like structures by tumor cells independent of endothelial cells, supporting survival and metastasis.

Why study FAK and ILK in relation to VM?

The study targets FAK and ILK because identifying genes involved in VM can support targeted therapy development against breast cancer metastasis.

What did the results show about ILK and FAK expression?

ILK and FAK expression was significantly elevated in metastatic breast tumor cells, linking higher metastatic VM-forming ability to higher ILK/FAK levels.

Sep 21, 2026

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