Baizhen Dai

Affiliated Hospital of Guangdong Medical College Hospital

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Rongjing Zhang

Hefei National Center for Physical Sciences at Nanoscale

Liang Zhu

Shanghai Jiao Tong University

Qiyang Mao

Guangdong Medical College

Wenmei Su

Guangdong Medical College

Xuefeng Wang

Moffitt Cancer Center

Kangxian Wang

Affiliated Hospital of Guangdong Medical College Hospital

Biao Deng

Guangdong Medical College

Wang Wan

Dalian Institute of Chemical Physics

Guanzhou Lin

Peking University

Dong Wu

Affiliated Hospital of Guangdong Medical College Hospital

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Guangdong Medical College

Affiliated Hospital of Guangdong Medical College Hospital

Guangxi Medical University

Shanghai Jiao Tong University

Peking University

Shenzhen University

Hefei National Center for Physical Sciences at Nanoscale

University of Science and Technology of China

South China Agricultural University

Max Planck Institute for Intelligent Systems

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LINC00885 promotes the development of lung adenocarcinoma through AKT/MTOR/P70 signaling LINC00885 may regulate migration, proliferation, and invasion through the mTOR pathway in lung adenocarcinoma

Research Square (Research Square) (2024)

Wang Wan Dong Wu Baizhen Dai Kangxian Wang Biao Deng

Abstract Previous studies have demonstrated a role for long non-coding RNAs in lung adenocarcinoma (LUAD). Here, we found high expression levels of LINC00885 in LUAD, especially in middle and advanced stage disease, by RNA-sequencing analysis. This suggests that LINC00885 may be a potential prognostic biomarker of LUAD. Our functional experiments showed that knocking down LINC00885 expression with small interfering RNAs inhibited the growth, migration, invasion, and autophagy of LUAD cells, blocked cell cycle progression, and promoted cell apoptosis. Additionally, LINC00885 knockdown reduced the protein expression levels of p21, MET, p-mTOR, and p-p70, suggesting that LINC00885 may regulate the growth and metastasis of LUAD through these signaling pathways. Additional experiments revealed that an mTOR activator rescued the inhibited cell growth, invasion, and migration following LINC00885 knockdown. Together, these findings demonstrate that LINC00885 may promote LUAD by regulating p21, MET, and mTOR/p70 signal transduction. This study suggests that LINC00885 may be a prognostic biomarker and therapeutic target in LUAD.

mTORC2

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10.21203/rs.3.rs-4946723/v1

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LINC00885 promotes development of lung adenocarcinoma through AKT/mTOR/P70 signaling LINC00885 may regulate migration, proliferation, and invasion of lung adenocarcinoma through the mTOR pathway

Research Square (Research Square) (2024)

Liang Zhu Wang Wan Wenmei Su Baizhen Dai Kangxian Wang

Abstract Purpose Previous studies have demonstrated the role of long non-coding RNAs (lncRNAs) in lung adenocarcinoma (LUAD). Methods Results RNA sequencing analysis identified high LINC00885 expression levels in LUAD, especially in the middle and advanced stages. Our functional experiments showed that knocking down expression of LINC00885 using small interfering RNAs inhibited the growth, migration, invasion, and autophagy of LUAD cells, blocked cell cycle progression, and promoted apoptosis. LINC00885 knockdown also reduced protein expression levels of p21, MET, p-mTOR, and p-P70, suggesting that LINC00885 may regulate the growth and metastasis of LUAD through these signaling pathways. Further experiments revealed that an mTOR activator rescued inhibited cell growth, invasion, and migration following LINC00885 knockdown. Conclusion These findings demonstrate that LINC00885 may promote LUAD by regulating p21, MET, and mTOR/P70 signal transduction. They also suggest that LINC00885 may be a prognostic biomarker and therapeutic target in LUAD.

mTORC2

10.21203/rs.3.rs-3917639/v1

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