RDM1可能通过调节MCM2在透明细胞肾细胞癌中发挥致癌作用。

Li Xiuming, Liu Hui, Wei Yujie, Wang Anxin, Lv Chengcheng, Zeng Yu

Hebei Key Laboratory of Panvascular Diseases, Chengde, 067000, Hebei, China.

Department of Urology, Affiliated Hospital of Chengde Medical University, Chengde, 067000, Hebei, China.

Sci Rep. 2025 Jul 2;15(1):22649. doi: 10.1038/s41598-025-07230-z.

Kidney cancer may result from different gene mutations, each contributing to different histological subtypes and prognoses. RAD52 motif-containing 1 (RDM1) regulates multiple cancer pathways, but its role in ccRCC is unknown to date. According to our results, RDM1 expression increased in ccRCC cells, which was correlated to poor survival in ccRCC patients. Knockdown of RDM1 arrested the cell cycle, promoted cell apoptosis, and apparently suppressed ccRCC cell growth in vitro and in vivo. From the mechanism perspective, RDM1 drove MCM2 to modulate ccRCC cell cycle. Thus, RDM1 inhibition blocks cell cycle progression, suppresses ccRCC cell growth, and is a promising approach for treating ccRCC.

肾癌可能由不同的基因突变引起，每种突变导致不同的组织学亚型和预后。含RAD52基序1（RDM1）调节多种癌症通路，但迄今为止其在肾透明细胞癌（ccRCC）中的作用尚不清楚。根据我们的结果，RDM1在ccRCC细胞中的表达增加，这与ccRCC患者的不良生存相关。敲低RDM1可使细胞周期停滞，促进细胞凋亡，并在体外和体内明显抑制ccRCC细胞生长。从机制角度来看，RDM1驱动微小染色体维持蛋白2（MCM2）来调节ccRCC细胞周期。因此，抑制RDM1可阻断细胞周期进程，抑制ccRCC细胞生长，是一种有前景的ccRCC治疗方法。