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氯化镧通过PI3K/Akt信号通路增强卵巢癌细胞对顺铂的耐药性。

Lanthanum Chloride Sensitizes Cisplatin Resistance of Ovarian Cancer Cells PI3K/Akt Pathway.

作者信息

Fang Shanyu, Zhang Ping, Chen Xinping, Liu Fujun, Wang Fen

机构信息

Department of Obstetrics and Gynecology, The First Affiliated Hospital of Nanchang University, Nanchang, China.

Department of Otorhinolaryngology Head and Neck Surgery, Jiujiang University Clinical Medical College, Jiujiang University Hospital, Jiujiang, China.

出版信息

Front Med (Lausanne). 2021 Dec 15;8:776876. doi: 10.3389/fmed.2021.776876. eCollection 2021.

Abstract

Our previous study manifested that lanthanum chloride (LaCl) can enhance the anticancer ability of cisplatin (DDP) in ovarian cancer cells. Here, ovarian cancer cells SKOV3 and SKOV3/DDP were subjected to DDP and LaCl. Cell viability, apoptosis, DNA repair, and PI3K/Akt pathway were detected. LaCl induced more cell death and apoptosis caused by DDP in two cell lines, accompanied by upregulation of Bax and Cleaved caspase 3 proteins, and downregulation of Bcl-2 protein. LaCl also could decrease RAD51 protein by inactivation of the PI3K/Akt pathway. These data indicated that LaCl could be a potential drug to modulate DDP resistance by inactivating of PI3K/Akt pathway and attenuating DNA repair in ovarian cancer.

摘要

我们之前的研究表明,氯化镧(LaCl)可增强顺铂(DDP)对卵巢癌细胞的抗癌能力。在此,将卵巢癌细胞SKOV3和SKOV3/DDP分别用DDP和LaCl处理。检测细胞活力、凋亡、DNA修复及PI3K/Akt通路。在两种细胞系中,LaCl诱导由DDP引起的更多细胞死亡和凋亡,同时伴有Bax和裂解的半胱天冬酶3蛋白上调,以及Bcl-2蛋白下调。LaCl还可通过使PI3K/Akt通路失活来降低RAD51蛋白水平。这些数据表明,LaCl可能是一种通过使PI3K/Akt通路失活和减弱卵巢癌DNA修复来调节DDP耐药性的潜在药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1026/8714849/a416bbdbf5cd/fmed-08-776876-g0001.jpg

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