ABSTRACT
Dendrobium nobile Lindl. alkaloids (DNLA) promote the apoptosis of breast cancer and colon cancer cells, but whether they affect the malignant biological behavior of cervical cancer cells is unknown. Herein we explored the effects and possible mechanisms of DNLA on the proliferation, apoptosis, migration and invasion of cervical cancer SiHa cells. SiHa cells were transfected with si-NC, siKCNQ1OT1, miR-NC, miR-487a-3p mimics, pcDNA-NC or pcDNA-KCNQ1OT1. Different doses (15, 30, 60 ng/mL) of DNLA were applied. The CCK-8 method was used to detect cell proliferation; Tran-swell was used to detect cell migration and invasion; flow cytometry was used to detect cell apoptosis; Western blotting was used to detect the expression of MMP2, MMP9 and Cleaved-Caspase-3 genes at the protein level; RT-qPCR was used to detect the expression of KCNQ1OT1 and miR-487a-3p. The dual luciferase reporter gene experiment verified the regulatory relationship between KCNQ1OT1 and miR-487a-3p. The results showed that different doses (15, 30, 60 ng/mL) of DNLA reduced the absorbance value, migration number, invasion number, the protein level of MMP2 and MMP9, reduced the expression of KCNQ1OT1, and increased the apoptosis rate, the abundance of Cleaved-Caspase-3 and the expression of miR-487a-3p (P<0. 05). Low expression of KCNQ1OT1 or high expression of miR-487a-3p reduced the absorbance value, migration number, invasion number, and the protein level of MMP2 and MMP9, but increased the apoptosis rate and the abundance of Cleaved-Caspase-3 (P<0. 05). KCNQ1OT1 negatively regulated the expression of miR-487a-3p. The effects of high expression of KCNQ1OT1 on the proliferation, apoptosis, migration and invasion of SiHa cells were opposite to that of low expression of KCNQ1OT1, and high expression of KCNQ1OT1 reduced the effects of 60 ng/mL DNLA on the proliferation, apoptosis, migration and invasion of SiHa cells. In summary, DNLA may reduce the proliferation, migration and invasion of cervical cancer SiHa cells and promote SiHa cell apoptosis by regulating the KCNQ1OT1/miR-487a-3p axis.