Hyperforin Suppresses Oncogenic Kinases and Induces Apoptosis in Colorectal Cancer Cells

Abstract

Background/aim: Signal transducer and activator of transcription 3 (STAT3), Janus Kinase 1 (JAK1), extracellular signal-regulated kinase (ERK), and protein kinase B (AKT) are essential for malignant transformation and progression in colorectal cancer (CRC) and can be considered as targets for therapeutic interventions. Hyperforin, an active constituent from Hypericum perforatum, has been reported to inhibit inflammation. However, whether hyperforin may suppress CRC progression via inactivation of JAK/STAT3, ERK or AKT signaling remains unclear.

Materials and methods: Human CRC cells were used to identify the treatment efficacy of hyperforin and its underlying mechanisms of action by MTT, flow cytometry, wound healing, and western blotting assays.

Results: Hyperforin not only induced cytotoxicity, extrinsic/intrinsic apoptosis signaling, but also suppressed the invasion/migration ability of CRC. The phosphorylation of STAT3, JAK1, ERK and AKT was found to be decreased by hyperforin.

Conclusion: Hyperforin inactivates multiple oncogenic kinases and induces apoptosis signaling in CRC cells.

Keywords: AKT; ERK; Hyperforin; JAK1; STAT3; apoptosis; colorectal cancer cells; oncogenic kinases.