Abstract
Gastric cancer remains a serious threat to human health worldwide. Kaempferol is a plant-derived flavonoid compound with a wide range of pharmacological activities. This study aimed to investigate the effects of kaempferol on gastric cancer SNU-216 cell proliferation, apoptosis, and autophagy, as well as underlying potential mechanisms. Viability, proliferation, and apoptosis of SNU-216 cells after kaempferol treatment were evaluated using cell counting kit-8 assay, 5-btomo-2′-deoxyuridine incorporation assay, and annexin V-FITC/PI staining, respectively. Quantitative reverse transcription PCR was performed to measure the mRNA expressions of cyclin D1 and microRNA-181a (miR-181a) in SNU-216 cells. Cell transfection was used to down-regulate the expression of miR-181a. The protein expression levels of cyclin D1, bcl-2, bax, caspase 3, caspase 9, autophagy-related gene 7, microtubule-associated protein 1 light chain 3-I (LC3-I), LC3-II, Beclin 1, p62, mitogen-activated protein kinase (MAPK), extracellular regulated protein kinases (ERK), and phosphatidylinositol 3 kinase (PI3K) in SNU-216 cells were detected using western blotting. Results showed that kaempferol significantly suppressed SNU-216 cell viability and proliferation but had no influence on cell apoptosis. Further results suggested that kaempferol significantly induced SNU-216 cell autophagy. The expression of miR-181a in SNU-216 cells after kaempferol treatment was enhanced. Kaempferol significantly inactivated MAPK/ERK and PI3K pathways in SNU-216 cells. Suppression of miR-181a significantly reversed the kaempferol-induced MAPK/ERK and PI3K pathways inactivation in SNU-216 cells. This research demonstrated that kaempferol suppressed proliferation and promoted autophagy of human gastric cancer SNU-216 cells by up-regulating miR-181a and inactivating MAPK/ERK and PI3K pathways.
Highlights
Gastric cancer is a major health burden worldwide, which accounts for roughly 28,000 new cases and 10,960 deaths per year [1,2]
These findings indicated that kaempferol could inactivate mitogen-activated protein kinase (MAPK)/extracellular regulated protein kinases (ERK) and phosphatidylinositol 3 kinase (PI3K) pathways in gastric cancer SNU-216 cells
These findings suggested that miR-181a played critical roles in kaempferol-induced MAPK/ERK and PI3K pathways inactivation in gastric cancer SNU-216 cells
Summary
Gastric cancer is a major health burden worldwide, which accounts for roughly 28,000 new cases and 10,960 deaths per year [1,2]. Searching for novel and more effective preventive, diagnostic, and therapeutic strategies for gastric cancer are still extremely needed. Regarding its anti-cancer effects, several preliminary studies demonstrated that kaempferol suppressed the growth of multiple cancers, including breast cancer [11], lung cancer [12], colon cancer [13], bladder cancer [14], hepatic cancer [15], pancreatic cancer [16], and gastric cancer [17]. More experimental research is still needed to further explore the specific molecular mechanisms of kaempferol on gastric cancer cells
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