astragalin and Stomach-Neoplasms

Abnormal glycosylation of cancer cells is considered a key factor of carcinogenesis related to growth, proliferation, migration and invasion of tumor cells. Many plant-based polyphenolic compounds reveal potential anti-cancer properties effecting cellular signaling systems. Herein, we assessed the effects of phenolic acid,

Topics: Coumaric Acids; Flavonoids; Fucosyltransferases; Humans; Kaempferols; NF-kappa B; Stomach Neoplasms

To investigate the effects and related molecular mechanisms of Astragalin on undifferentiated gastric cancer cell HGC-27.. Astragalin was used to treat HGC-27 cells, the cell proliferation activity was detected by CCK-8 method, the cell morphology was observed under inverted microscope, hoechst 33342 and JC-1 staining were used to observe the changes of nucleus formation and mitochondrial membrane potential, the cell cycle and apoptosis rate were detected by flow cytometry, the reverse transcription level of the gene was analyzed by the second-generation sequencer.. Astragalin inhibited the proliferation of HGC-27 significantly (. The apoptosis of undifferentiated gastric cancer cell line HGC-27 can be induced by Astragalin through inhibition of EGFR/PDK/Akt signaling pathway, and the cell cycle can be blocked in G1 phase, which has a certain therapeutic effect on undifferentiated gastric cancer.

Topics: Apoptosis; bcl-2-Associated X Protein; Cell Line, Tumor; Cell Proliferation; ErbB Receptors; Humans; Proto-Oncogene Proteins c-akt; Stomach Neoplasms

Gastric cancer is a common malignant cancer, which is one of the most affected cancers by PI3K/AKT signaling. Here, we investigated the anti-tumor role of Astragalin, a natural flavonoid compound, in gastric cancer and explored the underlying molecular mechanism. Three well-established gastric cancer cell lines and xenograft mouse model were used to examine the anti-tumor effect of Astragalin by using CCK-8, transwell assays, and Western blot. Tumor burden of xenograft mice with Astragalin administration was monitored and determined during and at end of the experiments. Astragalin could effectively inhibit cell viability of gastric cancer cells and possessed good anti-tumor activity in xenograft mice. In addition, astragalin induced the expression of apoptotic signaling proteins, suppressed the migration and invasion cancer cells, and inhibited the PI3K/AKT signaling pathway significantly. In contrast, epidermal growth factor stimulation was able to block the anti-tumor activity of Astragalin. In conclusion, astragalin exerts its anticancer activities through inhibiting PI3K/AKT signaling, which highlights its potential for the treatment of gastric cancer.

Topics: Animals; Antineoplastic Agents; Apoptosis; Cell Line, Tumor; Cell Proliferation; Flavonoids; Humans; Kaempferols; Mice; Mice, Nude; Phosphatidylinositol 3-Kinases; Phosphoinositide-3 Kinase Inhibitors; Protein Kinase Inhibitors; Protein Kinases; Proto-Oncogene Proteins c-akt; Signal Transduction; Stomach Neoplasms; Xenograft Model Antitumor Assays