@Article{or.2026.067601,
AUTHOR = {Hui Zha, Chao Li, Jia Chen, Hao Bo, Zhaolan Hu, Zailong Qin, Jie Guo, Junbin Yuan},
TITLE = {Multi-Scale Transcriptomic Sequencing Data Analysis Reveals <i>LINC00467</i> is Associated with Malignant Progression in Breast Cancer: An <i>In Silico</i> and <i>In Vitro</i> Study},
JOURNAL = {Oncology Research},
VOLUME = {34},
YEAR = {2026},
NUMBER = {4},
PAGES = {--},
URL = {http://www.techscience.com/or/v34n4/66662},
ISSN = {1555-3906},
ABSTRACT = { <b>Objective:</b> Long non-coding RNAs have been found to play a pivotal role in breast cancer, yet the majority of these lncRNAs remain to be thoroughly investigated. This study aimed to explore the role of differentially expressed long non-coding RNAs (lncRNAs) in breast cancer stemness and drug sensitivity. <b>Methods:</b> Database mining was performed to evaluate the expression of <i>LINC00467</i> in different types of breast cancer and its association with clinical features. The function of <i>LINC00467</i> was examined through colony formation assays, quantitative reverse transcription PCR (qRT-PCR), and western blotting following <i>LINC00467</i> silencing in breast cancer cell lines. <b>Results:</b> <i>LINC00467</i> was significantly upregulated in various breast cancer subtypes with spatial specificity. Silencing <i>LINC00467</i> reduced clonogenic capacity and downregulated the stemness-associated factor <i>LIN28B</i> as well as phosphorylated RAC-alpha serine/threonine-protein kinase (p-AKT). The transcription factors specificity protein 1 (<i>SP1</i>) and E2F transcription factor 1 (<i>E2F1</i>) were predicted to bind to the <i>LINC00467</i> promoter. Furthermore, breast cancer samples with high <i>LINC00467</i> expression displayed reduced sensitivity to AKT inhibitors, and high <i>LINC00467</i> expression was negatively correlated with the therapeutic response to programmed cell death 1 (PD-1) antibodies. <b>Conclusion:</b> Our findings suggest that spatially expressed <i>LINC00467</i> may promote breast cancer stemness by regulating AKT signaling and could serve as a potential new therapeutic target and indicator of drug sensitivity in breast cancer.},
DOI = {10.32604/or.2026.067601}
}