Farhad Mohammad, Rolig Annah S, Redmond William L
Earle A. Chiles Research Institute, Providence Portland Medical Center, Portland, OR.
Cell, Developmental, and Cancer Biology Department, Oregon Health and Science University, Portland, OR.
Oncoimmunology. 2018 Feb 20;7(6):e1434467. doi: 10.1080/2162402X.2018.1434467. eCollection 2018.
The efficacy of cancer immunotherapy is limited, in part, by the multitude of immunosuppressive mechanisms present within the tumor microenvironment (TME). Galectin-3 (Gal-3) is a lectin that contributes to TME immunosuppression and regulates diverse functions including cellular homeostasis and cancer biology. Increased Gal-3 expression during cancer progression augments tumor growth, invasiveness, metastatic potential, and immune suppression, which highlights the potential use of Gal-3 as a therapeutic target capable of modulating anti-tumor immunity. Here, we discuss the mechanisms by which Gal-3 regulates lymphocytes, the role of Gal-3 in lung and prostate tumors, and the contribution of Gal-3 to TME immunosuppression.
癌症免疫疗法的疗效受到一定限制,部分原因在于肿瘤微环境(TME)中存在多种免疫抑制机制。半乳糖凝集素-3(Gal-3)是一种凝集素,它有助于TME免疫抑制,并调节包括细胞内稳态和癌症生物学在内的多种功能。癌症进展过程中Gal-3表达增加会促进肿瘤生长、侵袭性、转移潜能和免疫抑制,这凸显了Gal-3作为能够调节抗肿瘤免疫的治疗靶点的潜在用途。在此,我们讨论Gal-3调节淋巴细胞的机制、Gal-3在肺癌和前列腺癌中的作用,以及Gal-3对TME免疫抑制的影响。