Silencing lnc-ASAH2B-2 Inhibits Breast Cancer Cell Growth via the mTOR Pathway.

Background/Aim: Persistent activation of the phosphatidylinositol-3-kinase/protein kinase B/mammalian target of rapamycin (mTOR) pathway is an important mechanism in resistance of breast cancer to endocrine therapy. Although everolimus has potent inhibitory effects on the mTOR pathway, it has demonstrated only modest clinical activity as a single agent. Whether long noncoding (Inc) RNA is involved in everolimus resistance is unknown. Materials and Methods: Cell viability, colony formation and cell proliferation experiments were used to measure the effects of long noncoding RNA N-acylsphingosine amidohydrolase 2B-2 (lnc-ASAH2B-2) knockdown in BT474 and MCF7 breast cancer cells. Results: lnc-ASAH2B-2 was up-regulated by everolimus in cells with and without serum, and reduction of lnc-ASAH2B-2 expression was able to inhibit proliferation of BT474 and MCF7 cells. Conclusion: lnc-ASAH2B-2 was up-regulated after everolimus exposure and efficiently regulated breast cancer cell growth by activating the mTOR pathway, which may reduce the effect of everolimus, providing evidence that lnc-ASAH2B-2 might be a new therapeutic target for breast cancer.