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Polydopamine-Coated Surfaces Promote Adhesion, Migration, Proliferation, Chemoresistance, Stemness, and Epithelial-Mesenchymal Transition of Human Prostate Cancer Cell Lines In Vitro via Integrin αβ-FAK-JNK Signaling.

International journal of molecular sciences 2026 Vol.27(2)

Song WH, Kim JE, Rajbongshi L, Lee SR, Kim Y, Hwang SY, Oh SO, Kim BS, Lee D, Yoon S

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Polydopamine (PDA) surface coatings are widely used in biomedical engineering to enhance cell-substrate interactions; however, their effects on cancer-cell behavior remain unclear.

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APA Song WH, Kim JE, et al. (2026). Polydopamine-Coated Surfaces Promote Adhesion, Migration, Proliferation, Chemoresistance, Stemness, and Epithelial-Mesenchymal Transition of Human Prostate Cancer Cell Lines In Vitro via Integrin αβ-FAK-JNK Signaling.. International journal of molecular sciences, 27(2). https://doi.org/10.3390/ijms27020655
MLA Song WH, et al.. "Polydopamine-Coated Surfaces Promote Adhesion, Migration, Proliferation, Chemoresistance, Stemness, and Epithelial-Mesenchymal Transition of Human Prostate Cancer Cell Lines In Vitro via Integrin αβ-FAK-JNK Signaling.." International journal of molecular sciences, vol. 27, no. 2, 2026.
PMID 41596307

Abstract

Polydopamine (PDA) surface coatings are widely used in biomedical engineering to enhance cell-substrate interactions; however, their effects on cancer-cell behavior remain unclear. In this study, we investigated how PDA-coated two-dimensional (2D) culture surfaces influence oncogenic traits of human prostate cancer (PC) cells in vitro. Using LNCaP, DU145, and PC3 cell lines, we found that PDA-coated substrates markedly increased the adhesion, migration, invasion, proliferation, and colony formation in a dose- and time-dependent manner. PDA exposure also induced epithelial-mesenchymal transition (EMT), upregulated cancer stem cell markers (, , , , , and ), and elevated expression of metastasis- and chemoresistance-associated molecules (, , , and ). Mechanistically, PDA coatings enhanced integrin αβ-associated cell adhesion, accompanied by increased focal adhesion kinase (FAK) phosphorylation and downstream activation of JNK signaling. Pharmacological inhibition of integrin αβ (BTT-3033), FAK (PF573228) and JNK (SP600125) effectively abrogated PDA-induced malignant phenotypes and restored chemosensitivity to cabazitaxel, cisplatin, docetaxel, curcumin, and enzalutamide. Collectively, these findings identify PDA-coated surfaces as a simple, efficient, and reductionist in vitro platform for studying adhesion-mediated signaling and phenotypic plasticity in PC cells, while acknowledging that further validation in three-dimensional (3D) and patient-derived models will be required to establish in vivo relevance.

MeSH Terms

Humans; Male; Indoles; Cell Movement; Epithelial-Mesenchymal Transition; Cell Adhesion; Prostatic Neoplasms; Drug Resistance, Neoplasm; Cell Proliferation; Neoplastic Stem Cells; Polymers; Cell Line, Tumor; Integrin alpha2beta1; MAP Kinase Signaling System; Signal Transduction; Focal Adhesion Kinase 1

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