Tubeimoside‑1 inhibits the proliferation and metastasis by promoting miR‑126‑5p expression in non‑small cell lung cancer cells
| Autor: | Ruizhi Gao, Hongxia Bi, Xingyuan Sun, Wei Li, Haiying Dong, Jiang Su, Haijun Mu, Yunfei Jiang, Hanbing Shi, Guohua Liu |
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| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
MAPK/ERK pathway Cancer Research Oncogene Kinase Chemistry Articles Cell cycle medicine.disease VEGF-A Metastasis Vascular endothelial growth factor miR-126-5p 03 medical and health sciences chemistry.chemical_compound 030104 developmental biology 0302 clinical medicine Oncology tubeimoside-1 030220 oncology & carcinogenesis microRNA Cancer research medicine Lung cancer non-small cell lung cancer |
| Zdroj: | Oncology Letters |
| ISSN: | 1792-1082 1792-1074 |
| DOI: | 10.3892/ol.2018.9051 |
| Popis: | Tubeimoside-1 (TBMS1) possesses broad anticancer activities, including the cytostatic and anti-angiogenesis effects in lung cancer. However, the effect of TBMS1 on the metastasis of non-small cell lung cancer (NSCLC) cells and the potential underlying mechanism remain unclear. In the present study, a cell counting kit-8 assay revealed that TBMS1 suppressed the proliferation of NCI-H1299 cells significantly, particularly following 48 h of treatment. Further studies showed that TBMS1 notably enhanced the apoptosis, and inhibited the migration and invasion of NCI-H1299 cells upon treatment for 48 h. A total of 14 NSCLC tissues and 14 normal adjacent tissues were collected, reverse transcription-quantitative polymerase chain reaction revealed decreased expression of microRNA (miR)-126-5p in NSCLC tissues compared with adjacent NSCLC tissues, which was reversed following TBMS1 administration in NCI-H1299 cells. The overexpression of miR-126-5p induced by TBMS1 was demonstrated to target and downregulate vascular endothelial growth factor (VEGF)-A. Simultaneously, the expression of VEGF-R2 was reduced notably, along with a significant declined in the phosphorylation levels of dual specificity mitogen-activated protein kinase kinase 1 and extracellular signal-regulated kinase (ERK)1/2. Overall, the aforementioned results indicated that TBMS1 inhibited the proliferation and metastasis, and promoted the apoptosis of NCI-H1299 cells, which may be mediated by overexpressing miR-126-5p, which inactivates the VEGF-A/VEGFR2/ERK signaling pathway. Therefore, TBMS1 may be a promising drug for prevention and treatment of NSCLC. |
| Databáze: | OpenAIRE |
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