LIMD2的敲低通过ERK1/2途径抑制卵巢癌的进展。
Knockdown of LIMD2 inhibits the progression of ovarian carcinoma through ERK1/2 pathway.
发表日期：2023 Sep 16
作者：
Haiyang Hu, Yanan Wang, Yan Dong, Lin Wang, Yahui Chen, Yan Zhou, Lin Sun
来源：
Cell Death & Disease
摘要：
卵巢癌(OC)的发病率在女性生殖系统恶性肿瘤中排名第三，而其死亡率在全球女性生殖系统肿瘤相关死因中排名第一。在本研究中，我们通过LIMD2的敲低研究了其在OC细胞中的特定作用。在线分析和表达检测的结果证明，LIMD2在人类OC组织和细胞中上调表达。LIMD2的敲下抑制了OC细胞的增殖、迁移和侵袭。LIMD2的敲下促进了细胞凋亡，以及Cleaved-Caspase3和Bax的表达。重要的是，LIMD2的敲下促进了细胞自噬。LIMD2敲下细胞中LC3-II/I比值和Beclin1的表达增加，而P62的表达减少。此外，LIMD2的敲下抑制了SKOV3和OVCAR3细胞中ERK1/2的磷酸化。LIMD2的敲下通过ERK1/2信号通路抑制了细胞增殖、迁移、侵袭和自噬，并促进了细胞凋亡，表明LIMD2-siRNA可能是预防OC进展的有效分子。© 2023. 本文作者独家授权给Springer Nature B.V.
The incidence rate of ovarian carcinoma (OC) is the third of the female reproductive system malignant tumors, while its mortality rate ranks first among causes of female reproductive system tumor related death in the world.In the present research, we investigated the specific role of LIMD2 through LIMD2 knockdown in OC cells.The results of online analysis and expression detection proved that LIMD2 was up-regulated in human OC tissues and cells. Knockdown of LIMD2 inhibited the proliferation, migration and invasion in OC cells. LIMD2 knockdown promoted the apoptosis, as well as the expression of Cleaved-Caspase3 and Bax. Importantly, knockdown of LIMD2 promotes cell autophagy. LC3-II/I ratio and Beclin1 expression increased in LIMD2 knockdown cells, while P62 expression declined in LIMD2 knockdown cells. Additionally, the phosphorylation of ERK1/2 was inhibited by the knockdown of LIMD2 in SKOV3 and OVCAR3 cells.Knockdown of LIMD2 inhibits cell proliferation, migration, invasion and autophagy, and promotes the apoptosis through the ERK1/2 signaling pathway, suggesting that LIMD2-siRNA may be an effective molecule to prevent OC progression.© 2023. The Author(s), under exclusive licence to Springer Nature B.V.