ESM1 promote proliferation, invasion and angiogenesis via Akt/mTOR and Ras pathway in kidney renal clear cell carcinoma

被引:0
作者
Luo, Jianjun [1 ]
Yi, Ting [2 ,3 ]
Wang, Yong [1 ]
Song, Wei [1 ]
Gao, Zhiyong [1 ]
Wang, Jiansong [1 ]
Li, Yukun [2 ]
机构
[1] Hunan Normal Univ, Hunan Prov Peoples Hosp, Affiliated Hosp 1, Dept Urol, Changsha 410005, Hunan, Peoples R China
[2] Cent South Univ, Xiangya Hosp Zhuzhou, Zhuzhou Cent Hosp, Dept Assisted Reprod Ctr, Zhuzhou, Hunan, Peoples R China
[3] Cent South Univ, Xiangya Hosp Zhuzhou, Zhuzhou Cent Hosp, Dept Trauma Ctr, Zhuzhou, Hunan, Peoples R China
来源
SCIENTIFIC REPORTS | 2025年 / 15卷 / 01期
关键词
KIRC; ESM1; Akt/mTOR pathway; Ras pathway; Angiogenesis; BEVACIZUMAB;
D O I
10.1038/s41598-024-82400-z
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
The most common types of renal carcinoma is kidney renal clear cell carcinoma (KIRC). ESM1 is a secreted protein, which involved in, lipids and glucose metabolism, but their role in angiogenesis is contradictory in different disease, especially in KIRC. Bioinformatic analysis confirmed the ESM1 expression and prognosis in KIRC. IHC staining revealed protein expression of ESM1 in KIRC samples. The role of ESM1 in KIRC proliferation and migration were tested by MTT, EdU, transwell analysis. The role of its paracrine function in KIRC angiogenesis was tested by functional experiments. The downstream molecular mechanism of ESM1 were further elucidated by WB and functional experiments. ESM1 was significantly increased in KIRC with prognostic significance. ESM1 knockdown inhibited the invasiveness capability and viability of KIRC cell. The paracrine of ESM1 enhanced HUVECs proliferation and migration to format tube in KIRC cell conditional medium. ESM1 knockdown induced the inactivation of Akt/mTOR and Ras pathway to attenuate proliferation, migration, invasion and angiogenesis in KIRC. ESM1 was a key role in the tumor microenvironment (TME) of KIRC, which promoted the proliferation, migration, invasion, and angiogenesis by activating Akt/mTOR and Ras pathway. It is a potential therapeutic target for KIRC patients.
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页数:14
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