Liu Jialin, Hu Shengyun, Zhao Liangbo, Yang Yanmei, Wu Guanghua, Duan Yimeng, Ma Xinrui, Wang Peiwen, Zhang Zhiyong, Zong Hong
Department of Oncology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450001, China.
Department of Colorectal Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450000, China.
Mol Med. 2025 Jun 12;31(1):235. doi: 10.1186/s10020-025-01294-3.
Colorectal cancer is one of the most common malignant tumors worldwide. Colorectal cancer has a poor survival rate because it tends to metastasise to the liver and other organs. PELI2, an E3 ubiquitin ligase, is down-expressed in a variety of tumors. However, the role of PELI2 in colorectal cancer has not been revealed. In the present study, we found that expression level of PELI2 were reduced significantly in colorectal tumors compared with normal tissues. Patients with low level of PELI2 expression tended to have poor prognosis. Moreover, PELI2 decreased the proliferation, migration and anti-apoptosis of colorectal cancer cells in vitro. We also constructed xenograft tumor model to verify colorectal tumor growth slowed down after PELI2 overexpression. Transcriptome analysis suggested that PELI2 suppressed colorectal cancer progression via the MAPK signaling pathway. In brief, our study shows that PELI2 inhibits colorectal cancer development by MAPK signaling pathway.
结直肠癌是全球最常见的恶性肿瘤之一。结直肠癌的生存率较低,因为它容易转移至肝脏和其他器官。PELI2是一种E3泛素连接酶,在多种肿瘤中表达下调。然而,PELI2在结直肠癌中的作用尚未明确。在本研究中,我们发现与正常组织相比,结直肠癌组织中PELI2的表达水平显著降低。PELI2表达水平低的患者预后往往较差。此外,PELI2在体外可降低结直肠癌细胞的增殖、迁移能力并抑制其抗凋亡能力。我们还构建了异种移植肿瘤模型,以验证PELI2过表达后结直肠肿瘤生长减缓。转录组分析表明,PELI2通过丝裂原活化蛋白激酶(MAPK)信号通路抑制结直肠癌进展。简而言之,我们的研究表明PELI2通过MAPK信号通路抑制结直肠癌的发展。