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3-epi-bufotalin suppresses the proliferation in colorectal cancer cells through the inhibition of the JAK1/STAT3 signaling pathway

SANHUA LI1,2,#, QINGHONG KONG1,2,#, XIAOKE ZHANG1,2, XINTING ZHU1,3, CHUNBO YU3, CHANGYAN YU1,2, NIAN JIANG1,2, JING HUI1,2, LINGJIE MENG1,2,*, YUN LIU1,2,3,*
1 Guizhou Provincial College–Based Key Lab for Tumor Prevention and Treatment with Distinctive Medicines, Zunyi, 563000, China
2 Life Science Institute of Zunyi Medical University, Zunyi, 563000, China
3 School of Preclinical Medicine of Zunyi Medical University, Zunyi, 563000, China
* Corresponding Authors: LINGJIE MENG. Email: ; YUN LIU. Email:
(This article belongs to this Special Issue: Recent Advancement in Cancer Molecular Signaling)

BIOCELL 2022, 46(11), 2425-2432. https://doi.org/10.32604/biocell.2022.019916

Received 24 October 2021; Accepted 06 April 2022; Issue published 07 July 2022

Abstract

Traditional Chinese medicine (TCM) has been increasingly employed in the last decades in China for both preventing and treating a variety of cancers. 3-epi-bufotalin is an active ingredient of TCM “Chanpi” with anti-tumor potential. However, the effect and mechanism of 3-epi-bufotalin on colorectal cancers were not well disclosed. The present study demonstrated that 3-epi-bufotalin could reduce viability, trigger apoptosis, and block the cell cycle at the G2/M stage in colorectal cancer cell lines HT29, RKO, and COLO205 in vitro. Moreover, 3-epi-bufotalin inhibited the JAK1/STAT3 signaling pathway. These results indicated the anti-proliferation ability of 3-epi-bufotalin in colorectal cancer cells.

Keywords

3-epi-bufotalin; Colorectal cancer; JAK1/STAT3 signaling pathway; Apoptosis

Cite This Article

LI, S., KONG, Q., ZHANG, X., ZHU, X., YU, C. et al. (2022). 3-epi-bufotalin suppresses the proliferation in colorectal cancer cells through the inhibition of the JAK1/STAT3 signaling pathway. BIOCELL, 46(11), 2425–2432.



This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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