免疫细胞中的 Kindlin-3 对于抑制小鼠前列腺癌肿瘤生长是必需的。
Kindlin-3 in Immune Cells Is Required to Suppress Prostate Cancer Tumor Growth in Mice.
机构信息
Collaborative Research Program for Cell Adhesion Molecules, Shanghai University School of Life Sciences, Shanghai, P.R. China.
Versiti Blood Research Institute, Milwaukee, WI, U.S.A.
出版信息
Anticancer Res. 2022 Mar;42(3):1217-1220. doi: 10.21873/anticanres.15588.
BACKGROUND/AIM: Kindlins are essential integrin activators. Kindlin-1 and kindlin-2 are often concomitantly expressed in epithelial tumor cells and participate in regulating tumor malignancy. However, it remains unclear whether kindlin-3, the one expressed in immune cells, also plays a role in regulating tumor malignancy.
MATERIALS AND METHODS
To examine the role of kindlin-3 in different immune cells in regulating solid tumor growth, a xenograft model of prostate cancer tumor growth in genetically modified kindlin-3 mice was employed.
RESULTS
Disruption of crosstalk between kindlin-3 and integrins significantly promoted subcutaneous prostate cancer tumor growth in mice. Furthermore, deficiency of kindlin-3 in T cells and NK cells, but not myeloid cells and B cells, significantly enhanced prostate cancer tumor growth.
CONCLUSION
Tumor-killing leukocytes require Kindlin-3 for suppressing cancerous tumor growth, thus providing a novel anticancer mechanism.
背景/目的：Kindlins 是整合素激活物的必需组成部分。Kindlin-1 和 Kindlin-2 通常在上皮肿瘤细胞中同时表达，并参与调节肿瘤恶性程度。然而，Kindlin-3 在免疫细胞中表达，其是否也在调节肿瘤恶性程度方面发挥作用尚不清楚。
材料和方法
为了研究 Kindlin-3 在不同免疫细胞中调节实体瘤生长中的作用，采用了基因修饰的 Kindlin-3 小鼠的前列腺癌肿瘤生长异种移植模型。
结果
Kindlin-3 与整合素之间的相互作用的破坏显著促进了小鼠皮下前列腺癌肿瘤的生长。此外，Kindlin-3 在 T 细胞和 NK 细胞中的缺失，而不是髓样细胞和 B 细胞中的缺失，显著增强了前列腺癌肿瘤的生长。
结论
杀伤肿瘤的白细胞需要 Kindlin-3 来抑制癌症肿瘤的生长，从而提供了一种新的抗癌机制。
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