skullcapflavone-i has been researched along with Lung-Neoplasms* in 1 studies
1 other study(ies) available for skullcapflavone-i and Lung-Neoplasms
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Skullcapflavone I suppresses proliferation of human lung cancer cells via down-regulating microRNA-21.
Lung cancer is the most leading cause of cancer-related deaths worldwide. Skullcapflavone I is a flavone compound extracted from Scutellaria baicalensis Georgi (Wogon). The present study investigated the effects of skullcapflavone I on human lung cancer cell proliferation, as well as underlying possible mechanism.. Cell proliferation was detected using Trypan blue assay. Cell viability was measured using cell counting kit 8 (CCK-8) assay. Quantitative reverse transcription PCR (qRT-PCR) was performed to assess microRNA-21 (miR-21) expression. Cell transfection was conducted to enhance the levels of miR-21 and protein phosphatase 2A (PP2A). Western blotting was used to evaluate the expressions of proliferation cell nuclear antigen (PCNA), Cyclin D1, PP2A, phosphatidylinositol 3-kinase (PI3K), protein kinase 3 (AKT), mechanistic target of rapamycin (mTOR) and p70S6K.. Skullcapflavone I significantly suppressed the viability and proliferation of A549 and H1975 cells. The expressions of miR-21 in A549 and H1975 cells were drastically decreased after skullcapflavone I treatment. Overexpression of miR-21 remarkably reversed the skullcapflavone I-induced A549 cell viability inhibition. Moreover, skullcapflavone I enhanced the expression of PP2A in A549 cells. Skullcapflavone I inactivated PI3K/AKT/mTOR signaling pathway in A549 cells via up-regulating PP2A. Besides, skullcapflavone I treatment had no significant influence on human normal bronchial epithelial 16HBE cell viability, proliferation and apoptosis.. Skullcapflavone I exerted anti-cancer effect on lung cancer cells by down-regulating miR-21 expression, up-regulating PP2A expression and then inactivating PI3K/AKT/mTOR signaling pathway. Topics: A549 Cells; Cell Line; Cell Line, Tumor; Cell Proliferation; Cell Survival; Down-Regulation; Flavones; Gene Expression Regulation, Neoplastic; Humans; Lung Neoplasms; MicroRNAs; Phosphatidylinositol 3-Kinases; Protein Phosphatase 2; Proto-Oncogene Proteins c-akt; Signal Transduction; TOR Serine-Threonine Kinases | 2019 |