- Elucidation of the mechanism of the compound "ACA-28" that selectively induces cell death in cancer cells
- ACA-28 induces cell death of cancer cells and inhibits the growth by destroying tumor suppressor factors.
- Expectations for the development of anticancer drugs with less side effects that target brakes instead of accelerators for cancer cells
Higashiosaka, Osaka, Japan. January 28th, 2021
A research group led by Prof. Reiko Sugiura, the Department of Pharmaceutical Sciences, Faculty of Pharmacy, Kindai University (Higashi-Osaka, Osaka), has elucidated the mechanism of the compound "ACA-28" that induces cell death/ apoptosis only in cancer cells.
In many cancer cells, extracellular signal-regulated kinases (ERKs) are active to accelerate their growth, whereas tumor suppressor Dual‐specificity phosphatases (DUSPs) inhibit ERK function thus acting as a brake for cancer. Importantly, in some cancer cells, active ERK increases DUSP protein levels to stabilize the cell balance.
The research group found that the compound "ACA-28" disrupts the balance of cancer cells and induces apoptosis by reducing the DUSP protein levels. DUSP down‐regulation in ERK‐active cancer cells might have the potential as a novel cancer measure.
The research paper is available online in the Life Science magazine "Genes to Cells" published by The Molecular Biology Society of Japan on January 28, 2021 (Japan Standard Time).
Research paper title: Down-regulation of dual-specificity phosphatase 6, a negative regulator of oncogenic ERK signaling, by ACA-28 induces apoptosis in NIH/3T3 cells overexpressing HER2/ErbB2
Journal name: Genes to Cells (Impact factor: 1.922)
Authors: Yuki Kanda Ayami Mizuno Teruaki Takasaki Ryosuke Satoh Kanako Hagihara Takashi Masuko Yuichi Endo Genzoh Tanabe Reiko Sugiura
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