Oncogenic role of abnormal spindle‑like microcephaly‑associated protein in lung adenocarcinoma

• Published in: International journal of oncology Vol. 58; no. 5; p. 1
• Main Authors: Wang, Jiang, Liang, Jinghui, Li, Haixia, Han, Jingyi, Jiang, Jin, Li, Yongmeng, Feng, Zitong, Zhao, Renchang, Tian, Hui
• Format: Journal Article
• Language: English
• Published: Athens Spandidos Publications 01-05-2021; Spandidos Publications UK Ltd; D.A. Spandidos
• Subjects: Adenocarcinoma; Biotechnology; Cell cycle; Cell division; Chemotherapy; Development and progression; Gene expression; Health aspects; Lung cancer; Microcephaly; Proteins; Radiation therapy; RNA; Scientific equipment and supplies industry; Stem cells; Wound healing; United States
• ISSN: 1019-6439; 1791-2423
• DOI: 10.3892/ijo.2021.5203

Lung adenocarcinoma (LUAD) is a common malignant cancer worldwide. It is urgent to explore its underlying molecular mechanism and identify novel diagnostic biomarkers. Abnormal spindle-like microcephaly (ASPM) has recently received considerable attention due to its function in tumor progression. However, its role in LUAD is unclear. The present study aimed to explore the clinical role of ASPM in LUAD. Seven pairs of LUAD and adjacent normal tissues were collected to identify potential LUAD biomarkers using transcriptome sequencing. The association between ASPM expression and LUAD progression was evaluated using bioinformatics analysis and data obtained from clinical specimens. Using small interfering RNA technology, the function of ASPM was analyzed in the LUAD H1299 and A549 cell lines. Transcriptional profiling of ASPM-deficient H1299 cells was then performed to determine the downstream targets of ASPM. Using databases and clinical specimens, it was revealed that ASPM expression was frequently elevated in LUAD tissues, and this upregulation was highly associated with LUAD progression. ASPM served as an oncogenic regulator of LUAD cell proliferation and metastasis. Mechanistically, ASPM facilitated epithelial-mesenchymal transition (EMT) via the PI3K/AKT signaling pathway and 740 Y-P, an activator of this pathway, restored the migratory ability of ASPM-knockdown LUAD cells. The current study identified ASPM as an independent prognostic biomarker of LUAD that served an important oncogenic role in regulating LUAD cell metastasis by promoting EMT via the PI3K/AKT signaling pathway. Targeting ASPM may therefore be a therapeutic strategy for treating LUAD.