Xiaoyi Li
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Xiaoyi Li has a total of 8 co-authors. Here are the top co-authors by number of shared publications:
- Jingjing Zhao
Department of Cardiology, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China
1 shared publication - Jueheng Wu
Department of Microbiology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China
1 shared publication - Junchao Cai
Department of Immunology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China
1 shared publication - Shaobo Huang
Cancer Center Dongguan Key Laboratory of Precision Diagnosis and Treatment for Tumors Guangdong Engineering Research Center of Boron Neutron Therapy and Application in Malignant Tumors The Tenth Affiliated Hospital Southern Medical University (Dongguan People's Hospital) Dongguan China
1 shared publication - Tianyu Tao
Cancer Research Institute School of Basic Medical Sciences Southern Medical University Guangzhou China
1 shared publication - Weiqi Gu
Department of Microbiology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China
1 shared publication
Latest Publications
- Open Access
Cytoplasmic Clusterin Suppresses Lung Cancer Metastasis by Inhibiting the ROCK1-ERK Axis
Clusterin (CLU) is a heterodimeric glycoprotein that has been detected in diverse human tissues and implicated in many cellular processes. Accumulating evidence indicates that the expression of secreted CLU correlates with the progression of cancers. However, the molecular mechanisms underlying its tumor-suppressive roles are incompletely uncovered. In this study, we demonstrate that precursor CLU is widely downregulated in lung cancer tissue, in which secretory CLU proteins are slightly decreased. Impressively, overexpressing CLU potently inhibits the migration, invasion and metastasis of lung cancer cells, whereas silencing CLU promotes this behavior; however, it appears that secretory CLU fails to exert similar anti-metastatic effects. Interestingly, the cytoplasmic precursor CLU binds ROCK1 to abrogate the interaction between ROCK1 and ERK and impair ERK activity, leading to the suppression of lung cancer invasiveness. Meanwhile, the expression of CLU was remarkably diminished in lung cancer bone metastasis loci when compared with subcutaneous tumors in the mouse model and hardly detected in the bone metastasis loci of lung cancer patients when compared with the primary. These findings reveal a novel insight into the function and regulation of cytoplasmic CLU in lung cancer, which might be a potential target for the diagnosis and treatment of metastatic lung cancer.
Open AccessCytoplasmic Clusterin Suppresses Lung Cancer Metastasis by Inhibiting the ROCK1-ERK Axis
Clusterin (CLU) is a heterodimeric glycoprotein that has been detected in diverse human tissues and implicated in many cellular processes. Accumulating evidence indicates that the expression of secreted CLU correlates with the progression of cancers. However, the molecular mechanisms underlying its tumor-suppressive roles are incompletely uncovered. In this study, we demonstrate that precursor CLU is widely downregulated in lung cancer tissue, in which secretory CLU proteins are slightly decreased. Impressively, overexpressing CLU potently inhibits the migration, invasion and metastasis of lung cancer cells, whereas silencing CLU promotes this behavior; however, it appears that secretory CLU fails to exert similar anti-metastatic effects. Interestingly, the cytoplasmic precursor CLU binds ROCK1 to abrogate the interaction between ROCK1 and ERK and impair ERK activity, leading to the suppression of lung cancer invasiveness. Meanwhile, the expression of CLU was remarkably diminished in lung cancer bone metastasis loci when compared with subcutaneous tumors in the mouse model and hardly detected in the bone metastasis loci of lung cancer patients when compared with the primary. These findings reveal a novel insight into the function and regulation of cytoplasmic CLU in lung cancer, which might be a potential target for the diagnosis and treatment of metastatic lung cancer.