LYAR promotes the proliferation of non-small cell lung cancer and is associated with poor prognosis

• Published in: Folia histochemica et cytobiologica 2021-01, Vol.59 (4), p.282-290
• Main Authors: Lu, Xiao-Ning, Ju, Guan-Jun, Wang, Yu-Xin, Wang, Yong-Liang, Wang, Kun, Chen, Jian-Le, Cai, Wei, Zang, Qi-Wei
• Format: Article
• Language: English
• Subjects: A549 Cells; Antibodies; Apoptosis; Biotechnology; Biotin; Carcinoma, Non-Small-Cell Lung - genetics; Cell cycle; Cell Line, Tumor; Cell Proliferation; Cloning; Cyclin A; DNA nucleotidylexotransferase; DNA-Binding Proteins - genetics; Flow cytometry; Gene expression; Gene Expression Regulation, Neoplastic; Humans; Immunohistochemistry; Leukemia; Lung cancer; Lung Neoplasms - genetics; Medical prognosis; Non-small cell lung carcinoma; Nuclear Proteins - genetics; Ovarian cancer; Patients; Proteins; Small cell lung carcinoma; Starvation; Survival; Tissues; Tumors
• ISSN: 0239-8508; 1897-5631
• DOI: 10.5603/FHC.a2021.0030

The aim of the study was to investigate the clinical significance of Ly-1 antibody reactive clone (LYAR) in non-small-cell lung cancer (NSCLC). The expressions of LYAR at the protein level in representative paired NSCLC tumor tissues and adjacent non-tumor tissues were measured by Western blot and immunohistochemistry. Kaplan-Meier method was used to calculate the survival curve of patients with NSCLC. Cell Counting Kit-8 assay and flow cytometry were used to estimate the cell proliferation and cell cycle, respectively. Terminal-deoxynucleotidyl-transferase-mediated dUTP-biotin nick end labeling (TUNEL) assay was performed to detect cell apoptosis. LYAR was dramatically overexpressed in NSCLC tissues which were closely related to the survival of patients with NSCLC. In clinical studies, the expression of LYAR was related to the clinical stage, histological differentiation, and Ki-67 expression. A positive correlation was found between LYAR and Ki-67 expression by Spearman's correlation test. After serum starvation for 72 h, serum re-addition significantly increased the expression of LYAR, PCNA, and Cyclin A and promoted the cell cycle progression. LYAR knockdown inhibited the proliferation and induced the G0/G1 cell cycle arrest and apoptosis of A549 cells. The present study revealed the clinical significance of LYAR in NSCLC. LYAR might serve as a tumor promoter in NSCLC progression by promoting the proliferation and inhibiting the apoptosis of NSCLC cells. Inhibiting the expression of LYAR was considered as a potential novel therapeutic strategy for NSCLC.