PI3K/AKT/mTOR通路
基因敲除
蛋白激酶B
上皮-间质转换
癌症研究
SOX2
下调和上调
细胞生长
信号转导
医学
生物
细胞生物学
细胞培养
转录因子
基因
遗传学
作者
Hainan Zhao,Ermin Wang
标识
DOI:10.1186/s12935-025-03956-y
摘要
Abstract The aggressiveness of clear cell renal cell carcinoma (KIRC) plays a crucial role in patient prognosis. This study investigated the role of COL1A1 in KIRC progression and its underlying molecular mechanisms through bioinformatics analysis, in vitro experiments, and xenograft mouse models. COL1A1 expression was significantly upregulated in KIRC and correlated with poor patient outcomes. Knockdown of COL1A1 inhibited tumor cell proliferation, migration, and invasion in both in vitro and xenograft models, as well as suppression of epithelial-mesenchymal transition (EMT). Knockdown of COL1A1 also significantly reduced the protein levels of the stemness markers OCT4 and SOX2 in KIRC cells. Additionally, COL1A1 inhibition impaired activation of the PI3K/Akt signaling pathway. These findings underscore the pivotal role of the COL1A1/PI3K/Akt axis in KIRC progression and suggest potential therapeutic strategies targeting this pathway.
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