Downregulation of TM7SF4 inhibits cell proliferation and metastasis of A549 cells through regulating the PI3K/AKT/mTOR signaling pathway

• Published in: Molecular medicine reports Vol. 16; no. 5; pp. 6122 - 6127
• Main Authors: Yang, Xudong, Song, Xiaoming, Wang, Xiaohang, Liu, Xiangyan, Peng, Zhongmin
• Format: Journal Article
• Language: English
• Published: Greece D.A. Spandidos 01.11.2017; Spandidos Publications; Spandidos Publications UK Ltd
• Subjects: 1-Phosphatidylinositol 3-kinase; A549 Cells; Adaptor Proteins, Signal Transducing - genetics; AKT protein; Breast cancer; Carcinoma, Non-Small-Cell Lung - genetics; Carcinoma, Non-Small-Cell Lung - pathology; Care and treatment; Cell adhesion & migration; Cell growth; Cell Line, Tumor; Cell migration; Cell Movement - genetics; Cell proliferation; Cell Proliferation - genetics; Cellular proteins; Cellular signal transduction; Development and progression; Disease Progression; Down-Regulation - genetics; Etiology; Gene expression; Genetic aspects; Health aspects; Humans; Investigations; Kinases; Lung cancer; Lung Neoplasms - genetics; Lung Neoplasms - pathology; Medical prognosis; Membrane Proteins - genetics; Metastases; Metastasis; Mortality; Pathogenesis; phosphatidylinositol 3-kinase/AKT/mammalian target of rapamycin; Phosphatidylinositol 3-Kinases - genetics; Polymerase chain reaction; Proteins; Proto-Oncogene Proteins c-akt - genetics; Reverse transcription; Signal transduction; Signal Transduction - genetics; Thyroid cancer; TOR protein; TOR Serine-Threonine Kinases - genetics; transmembrane 7 superfamily member 4; United States > US
• ISSN: 1791-2997; 1791-3004
• DOI: 10.3892/mmr.2017.7324

Lung cancer is one of the most common types of malignant tumor worldwide. The etiology of lung cancer is complex and, although significant progress has been made in previous investigations, the molecular mechanism responsible for lung cancer remains to be fully elucidated. In the present study, the association between lung cancer and transmembrane 7 superfamily member 4 (TM7SF4) was investigated. Reverse transcription-quantitative polymerase chain reaction technology was used to detect the expression of TM7SF4, and it was expressed at a high level in lung cancer. Furthermore, by overexpressing and inhibiting the expression of TM7SF4, the present study compared cell proliferation and migration rates. It was confirmed that TM7SF4 promoted lung cancer cell proliferation and migration. TM7SF4 was also confirmed to promote cancer cell migration and invasion by modulating the activation of the phosphatidylinositol 3-kinase/Akt pathway in the A549 cells. Correspondingly, the inhibition of TM7SF4 decreased the expression of proteins associated with AKT, whereas the overexpression of TM7SF4 promoted the expression of the relevant proteins. Therefore, the present study confirmed that TM7SF4 was involved in the progression of lung cancer via regulating the activation of AKT. These findings suggested that TM7SF4 may be involved in the progression of lung cancer and may be a novel therapeutic target for this disease.