**4. Conclusions**

The results of the present study showed two beneficial e ffect of PN on KRAS-mutated CRC. Firstly, it significantly suppressed KRAS-mutated CRC progression. Cell proliferation and clonogenic potential were decreased at relatively low concentrations via apoptosis and G2/M phase arrest. The mechanism responsible for the e ffects of PN may be associated with the AKT/mTOR signaling pathway. Secondly, PN rescued muscle cells dysfunction under cancer progression. Collectively, our results provide support for the incorporation of PN into therapeutic regimens targeting mutated KRAS-driven CRC. For future research, the toxicity and e fficacy of PN needs to be performed in animal studies.

**Author Contributions:** J.S. carried out most of the experiments and contributed data interpretation; H.S. contributed to the experimental design and performed clonogenic potential and Western blot experiments; M.-R.K. contributed to data interpretation; S.-J.L. contributed to the conception; S.A. prepared compound PN and contributed to the conception; M.S. contributed to the conception and design of the entire study and wrote the manuscript. All authors have read and agreed to the published version of the manuscript.

**Funding:** This research was funded by Brain Korea 21 (NRF-2016R1A1A1A05921948) and by Basic Research of the NRF (NRF-2020R1F1A1076624). The APC was funded by NRF-2020R1F1A1076624.

**Acknowledgments:** The authors thank to KyungA Rhu and Heebang Cho on analyzing cell images.

**Conflicts of Interest:** The authors have nothing to declare.
