CircPTK2 accelerates tumorigenesis of colorectal cancer by upregulating AKT2 expression via miR‐506‐3p

Abstract

Abstract With the rapid increase in its incidence in the last decade, colorectal cancer (CRC) is becoming one of the most life‐threatening cancers. Circular RNA PTK2 (circPTK2) has multiple functions in oncogenesis, including in CRC. However, it remains elusive if circPTK2 also plays an important role in CRC malignancy. The levels of circPTK2, miR‐506‐3p, and AKT serine/threonine kinase 2 (AKT2) were measured by qPCR. The protein level of AKT2 was evaluated by western blotting assay. The proliferation, migration, and invasion of CRC cancer cells were evaluated by MTT, colony formation, wound‐healing, and transwell assays. The interaction between circPTK2 and miR‐506‐3p and between miR‐506‐3p and AKT2 mRNA were verified by dual‐luciferase reporter assay. The expressions of circPTK2 and AKT2 were elevated in CRC cells, with a concomitant reduction of miR‐506‐3p. The knockdown of circPTK2 suppressed the proliferation, migration, and invasion of CRC cells. CircPTK2 targeted miR‐506‐3p and negatively regulated its expression. Furthermore, miR‐506‐3p overexpression suppressed the CRC progression by downregulating the AKT2 expression. AKT2 overexpression or miR‐506‐3p inhibition restored the suppression of growth and invasiveness of CRC cancer cells caused by circPTK2 silencing. The circPTK2/miR‐506‐3p/AKT2 axis plays a novel and essential role in promoting CRC progression, providing potential targets for CRC therapeutic modality.

Keywords

• AKT2
• circPTK2
• colorectal cancer
• miR‐506‐3p