Abstract
Objective: The purpose of our research was to investigate the clinical significance of lncRNA VIM anti-sense 1 (VIM-AS1) and to elucidate its cellular functions in breast cancer patients. Methods: A cohort of one hundred and twenty-one individuals diagnosed with breast cancer and 95 healthy volunteers were recruited for this study. Relative abundances of VIM-AS1 were detected through quantitative real-time polymerase chain reaction (qRT-PCR). Receiver operating characteristic (ROC) was employed for evaluating the diagnosis potential of VIM-AS1. Kaplan-Meier method and Cox regression analysis was performed to further examine the prognostic performance of VIM-AS1. The cellular events of VIM-AS1 were assessed via CCK-8 and Transwell assay. The target interaction of VIM-AS1 and microRNA-29a-3p (miR-29a-3p) was verified via luciferase activity report assays. Results: VIM-AS1 expression was notably elevated in serum of breast cancer, demonstrating a significant diagnostic capacity for breast cancer patients. Its abnormal expression level was significantly correlated with TNM (tumor node metastasis, P = 0.020) and lymph node metastasis (P = 0.040). Moreover, a reduced overall survival rate was observed in patients exhibiting high VIM-AS1 expression (P = 0.001). Multivariate analysis illustrated that VIM-AS1 (P = 0.003, HR = 2.345, 95%CI = 1.340-4.103) was an independent prognostic biomarker for breast cancer patients, alongside TNM (P = 0.006; HR = 2.251; 95%CI = 1.24-4.009). Functionally, silencing VIM-AS1 resulted in the inhibition of key cell behaviors in vitro, including proliferation, migration and invasion. Besides, VIM-AS1 was found to negatively regulated miR-29a-3p, which may relieve the impacts of VIM-AS1 on breast cancer cells. Conclusion: VIM-AS1 exhibited aberrant expression in breast cancer, playing a critical role in tumor development by targeting miR-29a-3p. Our findings highlight the potential of VIM-AS1 as a novel diagnostic and prognostic biomarker in breast cancer. However, further in vivo studies and exploration of miR-29a-3p downstream targets are needed to fully elucidate the mechanistic role of VIM-AS1 in breast cancer progression.