Purpose: Despite the emergence of innovative cancer treatment strategies, the global burden imposed by malignant glioma is expected to increase. Therefore there is an immediate need to find novel and better approaches for its treatment. The main aim of the current research work was to evaluate the anticancer effects of naturally occurring catechin flavonoid along with examining its effects on cell autophagy, cell cycle phase distribution, cell migration and invasion and MAPK/ERK signalling pathway.
Methods: MTT cell viability assay was used to assess the effects on cell proliferation and clonogenic assay was used to assess the effects on cell colony formation. Transmission electron microscopy (TEM) and western blot assay were used to examine the effects on autophagy. Flow cytometry was used to assess the effects of catechin on cell cycle, while the effects on cell migration and cell invasion were examined by wound healing assay and transwell chambers assay. Effects on MAPK/ERK signalling pathway were assessed by western blot assay.
Results: The results indicated that catechin molecule led to significant and dose-dependent growth inhibitory effects on U87MG human glioma cells with lower cytotoxicity in normal astrocytes. Clonogenic assay indicated strong decrease in glioma cell colonies. TEM revealed that catechin induced autophagy in U87MG cells by creating autophagosomes and autophagic vacuoles. The catechin-triggered autophagy was also linked with increase in the expression of LC3II and decrease in p62 expression. However, moderate effects were observed on the LC3 I expression. Catechin also triggered G2/M phase cell cycle arrest along with inhibiting cell migration and invasion in a dose-dependent manner. This molecule also led to blocking of MAPK/ERK signalling pathway.
Conclusions: In conclusion, the results indicate that the naturally occurring catechin showed strong anticancer effects in U87MG human glioma cells by targeting autophagy, cell cycle, cell migration and invasion and targeting MAPK/ERK signalling pathway.