Guangquan Xu1, Yongchao Li1, Ruidong Zhu1, Pengcheng Song1, Youlei Wei1, Tian Liang2 and Tianze Zhang1*
1Department of Thoracic Surgery, The 2nd Affiliated Hospital of Harbin Medical University, China
2Department of Obstetrics and Gynaecology, The 1st Affiliated Hospital of Harbin Medical University, China
*Corresponding Author: Tianze Zhang, Department of Thoracic Surgery, the 2nd Affiliated Hospital of Harbin Medical University, China.
Received: September 24, 2020; Published: November 28, 2020
Non-small cell lung cancer is known as a malignant tumor with low survival rate and poor prognosis. Depression affects various diseases. However, the effect of depression on the progression of NSCLC remains unclear. In our current study, chronic mild stress (CMS) mice was used as depression animal model. Depression prompted the tumor progression in vivo analysis, including increasing tumor indexes and reducing survival rate. Serotonin secretion was observed to be remarkable elevation in both serum and tumor tissue, which was positively related with tumor progression. In vitro assays, serotonin promoted the proliferation of A549 cells. Additionally, we observed that miR-144 expression was significantly downregulated in serotonin stimulated group. Further loss-of- and gain-of-function assays verified that miR-144 was the downstream factor of serotonin underlying the condition of CMS. Taken together, our research indicated that CMS-induced serotonin secretion accelerates NSCLC proliferation via inhibiting miR-144 expression, suggesting the potential therapeutic direction in NSCLC patients.
Keywords: Depression; Chronic Mild Stress; miR-144; NSCLC
Citation: Tianze Zhang., et al. “Depression Accelerates Tumor Cell Proliferation Via Regulating Serotonin/miR-144 Axis in NSCLC Mice". Acta Scientific Pharmaceutical Sciences 4.12 (2020): 63-72.
Copyright: © 2020 Tianze Zhang., et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.