[HECTD2通过驱动LPCAT1的泛素化和降解抑制结直肠癌细胞增殖]
[HECTD2 Represses Cell Proliferation in Colorectal Cancer through Driving Ubiquitination and Degradation of LPCAT1].
作者信息
Ma L, Li D H, Xu Z
机构信息
Department of General Surgery, Qingdao Municipal Hospital, Qingdao University, 266000 China.
出版信息
Mol Biol (Mosk). 2022 Jul-Aug;56(4):574-584. doi: 10.31857/S0026898422040073.
Colorectal cancer (CRC) is a malignancy featured by a poor overall survival and a high recurrence rate, whereas the biomarkers for CRC remain to be investigated. Herein, it was found that lysophosphatidylcholine acyltransferase 1 (LPCAT1) was highly expressed in CRC, and LPCAT1 overexpression significantly promoted CRC cell proliferation, while it was reversed by LPCAT1 depletion. In addition, HECT domain-containing 2 (HECTD2) protein was determined as a post-translational mediator of LPCAT1 because HECTD2 co-immunoprecipitated with high ubiquitinated LPCAT1. Furthermore, upregulated LPCAT1 rescued the impairment of CRC cell proliferation caused by HECTD2 overexpression. In conclusion, our findings supported HECTD2/LPCAT1 axis as a potential prognostic biomarker in CRC.
结直肠癌（CRC）是一种总体生存率低且复发率高的恶性肿瘤，而CRC的生物标志物仍有待研究。在此，发现溶血磷脂酰胆碱酰基转移酶1（LPCAT1）在CRC中高表达，LPCAT1的过表达显著促进CRC细胞增殖，而LPCAT1的缺失则使其逆转。此外，含HECT结构域的2（HECTD2）蛋白被确定为LPCAT1的翻译后调节因子，因为HECTD2与高泛素化的LPCAT1共免疫沉淀。此外，上调的LPCAT1挽救了由HECTD2过表达引起的CRC细胞增殖损伤。总之，我们的研究结果支持HECTD2/LPCAT1轴作为CRC潜在的预后生物标志物。
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