Identification of a novel therapeutic target for lung cancer: Mitochondrial ribosome protein L9

被引:3
|
作者
Li, Xin-Yuan [1 ]
He, Xin-Yu [1 ]
Zhao, Hong [2 ]
Qi, Lu [1 ,3 ,6 ]
Lu, Jin-Jian [1 ,4 ,5 ,7 ]
机构
[1] Univ Macau, Inst Chinese Med Sci, State Key Lab Qual Res Chinese Med, Macau, Peoples R China
[2] First Affiliated Hosp Zhejiang Chinese Med Univ, Hangzhou 310006, Peoples R China
[3] Southern Med Univ, Sch Basic Med Sci, Dept Pathol, Guangzhou 510515, Peoples R China
[4] Univ Macau, Fac Hlth Sci, Dept Pharmaceut Sci, Macau, Peoples R China
[5] Univ Macau, Guangdong Hong Kong Macau Joint Lab Chinese Med &, Macau, Peoples R China
[6] Southern Med Univ, Sch Basic Med Sci, Dept Pathol, 1023 Shatai Rd, Guangzhou 510515, Guangdong, Peoples R China
[7] Univ Macau, Ave da Univ, Inst Chinese Med Sci, State Key Lab Qual Res Chinese Med, 5005a,N22, Macau, Peoples R China
关键词
MRPL9; Lung cancer; Bioinformatics; c-MYC; ZEB1; EPITHELIAL-MESENCHYMAL TRANSITION; CELL-PROLIFERATION; MYC; MRPL13; OVEREXPRESSION; TRANSCRIPTION; CHEMOTHERAPY; CONTRIBUTES; METASTASIS; DATABASE;
D O I
10.1016/j.prp.2023.154625
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
Lung cancer has a high fatality rate and incidence rate. At present, the initial and progress mechanism of lung cancer has not been completely elucidated and new therapeutic targets still need to be developed. In this study, the screening process was based on lung cancer expression profile data and survival analysis. Mitochondrial ribosome protein L9 (MRPL9) was upregulated in lung cancer tissues and related to the poor overall survival rate and recurrence-free survival rate of lung cancer patients. Knockdown of MRPL9 inhibited the proliferation, sphere-formation, and migration ability of lung cancer cells. MRPL9 was associated with the c-MYC signaling pathway, and lung cancer patients with high expression of both MRPL9 and MYC had a poor prognosis. Furthermore, c-MYC was associated with the epithelial-mesenchymal transition (EMT) regulatory protein zinc finger E-box binding homeobox 1 (ZEB1) by bioinformatics analysis. The relationship between ZEB1 and c-MYC was further confirmed by interfering with c-MYC expression. MRPL9 is a potential therapeutic target for lung cancer and exerts its biological functions by affecting the transcription factor c-MYC thereby regulating the EMT regulator ZEB1.
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页数:10
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