Combination of FAK inhibitor and cytokine-induced killer cell therapy: An alternative therapeutic strategy for patients with triple-negative breast cancer

doi:10.1016/j.biopha.2023.114732

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Title:	Combination of FAK inhibitor and cytokine-induced killer cell therapy: An alternative therapeutic strategy for patients with triple-negative breast cancer
Authors:	Wu, Cheng-Che Pan, Mei-Ren Shih, Shen-Liang Shiau, Jun -Ping Wu, Chun-Chieh Chang, Shu-Jyuan Kao, Chieh-Ni Chen, Fang -Ming Hou, Ming-Feng Luo, Chi-Wen
Contributors:	Kaohsiung Med Univ Hosp, Dept Surg, Div Breast Oncol & Surg Kaohsiung Med Univ, Grad Inst Clin Med Kaohsiung Med Univ Hosp, Ctr Canc Res Kaohsiung Med Univ Hosp, Dept Pathol Kaohsiung Med Univ, Coll Life Sci, Dept Biomed Sci & Environm Biol Kaohsiung Med Univ, Ctr Liquid Biopsy & Cohort Res Chia Nan Univ Pharm & Sci, Dept Cosmet Sci Chia Nan Univ Pharm & Sci, Inst Cosmet Scin Kaohsiung Med Univ Hosp, Dept Surg
Keywords:	Focal adhesion kinase (FAK) Cytokine-induced killer (CIK) cell Triple-negative breast cancer (TNBC) Adoptive cell therapy (ACT) Tumor microenvironment (TME)
Date:	2023
Issue Date:	2024-12-25 11:04:34 (UTC+8)
Publisher:	ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
Abstract:	Triple-negative breast cancer (TNBC) is characterized by the loss of expression of several biomarkers, which limits treatment strategies for the disease. In recent years, immunotherapy has shown promising results in the treatment of various tumors. Emerging evidence demonstrated that TNBC is an immune-activated cancer, sug-gesting that immunotherapy could be a feasible treatment option for TNBC. Cytokine-induced killer (CIK) cell therapy is considered as a potential treatment for cancer treatment. However, it is still not approved as a standard treatment in the clinical setting. Our previous study demonstrated that focal adhesion kinase (FAK) plays important role in regulating the sensitivity of TNBC cells to CIK cells. In this study, we further verify the role of FAK in regulating the immune response in vivo. Our in vitro study indicated that knockdown of FAK in TNBC cells or treat with the FAK inhibitor followed by co-culture with CIK cells induced more cell death than CIK cells treatment only. RNA-seq analysis indicated that suppression of FAK could affect several immune-related gene expressions in TNBC cells that affects the immune response in the tumor microenvironment of TNBC cells. The combination of FAK inhibitor and CIK cells significantly suppressed tumor growth than the treatment of FAK inhibitor or CIK cells alone in vivo. Our findings provide new insights into the cytotoxic effect of CIK cell therapy in TNBC treatment and indicate that the combination of CIK cell therapy with FAK inhibitors may be an alternative therapeutic strategy for patients with TNBC.
Relation:	Biomedicine & Pharmacotherapy, v.163, Article 114732
Appears in Collections:	[Offices] 456

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