International Master's Program of Biomedical Sciences, College of Medicine, China Medical University, Taichung 404328, Taiwan.
Department of Laboratory Hematology, Hanoi Medical University, Hanoi 11520, Vietnam.
Int J Mol Sci. 2022 Jan 21;23(3):1176. doi: 10.3390/ijms23031176.
TRIM37 dysregulation has been observed in several cancer types, implicating its possible role in tumorigenesis. However, the role of TRIM37 in pancreatic cancer progression remains unclear. In the present study, we observed that TRIM37 knockdown resulted in reduced proliferation, clonogenicity, migration, and invasion ability of pancreatic cancer cells. Furthermore, an in vivo study using an orthotopic syngeneic animal model further confirmed that reduced expression of TRIM37 in cancer cells suppressed tumor growth in vivo. Moreover, in mice bearing TRIM37 knockdown pancreatic cancer cells, the proportion of CD11bF4/80MHCII immunosuppressive macrophages was significantly reduced in tumor milieu, which might be due to the regulatory role of TRIM37 in cytokine production by pancreatic cancer cells. Collectively, these findings suggest a key role of TRIM37 in promoting pancreatic cancer progression.
TRIM37 失调已在多种癌症类型中观察到，提示其在肿瘤发生中可能发挥作用。然而，TRIM37 在胰腺癌进展中的作用尚不清楚。在本研究中，我们观察到 TRIM37 敲低导致胰腺癌细胞增殖、集落形成、迁移和侵袭能力降低。此外，使用原位同基因动物模型的体内研究进一步证实，癌细胞中 TRIM37 表达降低抑制了体内肿瘤生长。此外，在携带 TRIM37 敲低胰腺癌细胞的小鼠中，肿瘤微环境中 CD11bF4/80MHCII 免疫抑制性巨噬细胞的比例显著降低，这可能是由于 TRIM37 对胰腺癌细胞细胞因子产生的调节作用。综上所述，这些发现提示 TRIM37 在促进胰腺癌进展中起关键作用。
