Abstract
Cordyceps militaris is a commonly used medicinal mushroom containing various therapeutic effects such as anti-inflammatory, anti-allergic, and anti-cancer activities. This study examined whether Cordyceps militaris on germinated soybeans (GSC) has a suppressive effect on a v-ki-ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS)-driven colorectal cancer which is notorious for its un-druggable features and the ineffectiveness of conventional therapies against it. GSC extract was prepared and its proximate composition and amino acids were analyzed. The suppressive effects were investigated with the KRAS-driven colorectal cancer cell-line, SW480. SW480 proliferation, clonogenic potential, apoptosis, and the RAS/extracellular signal-regulated kinase (ERK) pathway under the GSC treatment were analyzed by 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) assay, flow cytometry, and Western blot, respectively. An in vivo experiment with the SW480 xenograft mouse model was performed. As a result, GSC suppressed cell proliferation by inducing the apoptosis of KRAS-driven colorectal cancer cells and inhibited clonogenic capabilities. The decrease of KRAS and ERK phosphorylation was detected by Western blot. Tumor growth was significantly suppressed when GSC was introduced to the tumor-xenograft mouse model. In conclusion, GSC suppressed KRAS-driven colorectal cancer growth both in vitro and in vivo, and can be used as an alternative or simultaneous approach in colorectal cancer therapy.
Highlights
Colorectal cancer (CRC) is the third most prevalent cancer worldwide [1]
30% to 40% of CRC patients have a v-ki-ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS)-driven CRC, which is difficult to target with drugs due to its notorious ‘un-druggable’ property
KRAS-driven colorectal cancer is initiated from the epidermal growth factor (EGF) binding to the EGF receptor (EGFR), which activates GTP-bound KRAS
Summary
Colorectal cancer (CRC) is the third most prevalent cancer worldwide [1]. Approximately1.7 million new cases were diagnosed in 2016 and 830,000 people were estimated to have died as a result [1]. Colorectal cancer (CRC) is the third most prevalent cancer worldwide [1]. The incidence of CRC is high in developed countries compared to developing countries, but the cases are increasing worldwide due to nutritional transitions. KRAS-driven colorectal cancer is initiated from the epidermal growth factor (EGF) binding to the EGF receptor (EGFR), which activates GTP-bound KRAS. The activated KRAS continuously transmits a signal to the downstream RAS-ERK cell regulation pathways. The ERK proteins activated by their phosphorylation are translocated to the nucleus and activate the transcription factors that involve the cell cycle progression and transcription. They are involved directly in tumor progression.
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