HOTTIP participates in mammary cancer by promoting cell proliferation via PI3K/AKT pathway.

Abstract

To investigate the role of HOTTIP in the development of mammary cancer and its underlying mechanism. 70 mammary cancer tissues and paracancerous tissues surgically resected from mammary cancer patients were enrolled in this study. HOTTIP expressions in these mammary cancer tissues and paracancerous tissues were detected by qRT-PCR (quantitative real-time polymerase chain reaction). The relationship between HOTTIP expression, prognosis, tumor size, and stage of mammary cancer patients was analyzed. Subsequently, we constructed lentivirus of HOTTIP. Proliferation, apoptosis, cell cycle, and invasion of mammary cancer cells transfected with HOTTIP lentivirus were detected by CCK-8 (cell counting kit-8), colony formation, flow cytometry, and transwell assay, respectively. The effect of overexpressed HOTTIP on PI3K/AKT pathway was detected by Western blot. HOTTIP was overexpressed in mammary cancer tissues than that of paracancerous tissues. HOTTIP expression was negatively correlated with the prognosis of mammary cancer. Overexpressed HOTTIP remarkably promoted cell cycle, and increased expressions of CyclineD1 and PCNA. Meanwhile, overexpressed HOTTIP inhibited cell apoptosis, whereas promoted proliferation and colony formation abilities. Western blot results demonstrated that overexpressed HOTTIP promotes proliferation of mammary cancer cells via PI3K/AKT pathway. HOTTIP remarkably promotes proliferative and invasive abilities, but inhibits cell apoptosis of mammary cancer cells via PI3K/AKT pathway.