<p>Colorectal cancer, a prevalent digestive system malignancy, is characterized by a high incidence, low early detection rate, limited surgical resection opportunities, and high mortality. Palmatine (PAL), an active ingredient primarily found in Coptidis Rhizoma, exhibits diverse pharmacological effects, including antibacterial, anti-inflammatory, and anti-tumor properties. While PAL has been shown to effectively curb the progression of colorectal cancer, the underlying mechanisms have yet to be fully elucidated. In this study, we demonstrated the inhibitory effect of PAL on colorectal cancer growth via the miR-363-3p/AURKA axis, utilizing an AOM/DSS-induced colorectal cancer model in C57BL/J mice, a subcutaneous tumor xenograft model in nude mice, and in vitro assays using HCT-116 and SW620 cells. PAL upregulates miR-363-3p expression, promotes the interaction between AURKA 3'UTR mRNA and miR-363-3p, impedes AURKA mRNA translation into AURKA protein, thereby inhibiting colorectal cancer cell proliferation and migration, and suppressing the initiation and progression of colorectal cancer. These results expand the understanding of the regulatory mechanisms by which PAL influences colorectal cancer development, and may provide new potential targets for colorectal cancer diagnosis and therapy.</p>

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Palmatine inhibits colorectal cancer proliferation and metastasis by regulating miR-363-3p/AURKA axis

  • Changxia Mao,
  • Xue Chai,
  • Huan He,
  • Jianyu Zhu,
  • Juan Li,
  • Hang Ma,
  • Xuegang Li,
  • Xiaoli Ye

摘要

Colorectal cancer, a prevalent digestive system malignancy, is characterized by a high incidence, low early detection rate, limited surgical resection opportunities, and high mortality. Palmatine (PAL), an active ingredient primarily found in Coptidis Rhizoma, exhibits diverse pharmacological effects, including antibacterial, anti-inflammatory, and anti-tumor properties. While PAL has been shown to effectively curb the progression of colorectal cancer, the underlying mechanisms have yet to be fully elucidated. In this study, we demonstrated the inhibitory effect of PAL on colorectal cancer growth via the miR-363-3p/AURKA axis, utilizing an AOM/DSS-induced colorectal cancer model in C57BL/J mice, a subcutaneous tumor xenograft model in nude mice, and in vitro assays using HCT-116 and SW620 cells. PAL upregulates miR-363-3p expression, promotes the interaction between AURKA 3'UTR mRNA and miR-363-3p, impedes AURKA mRNA translation into AURKA protein, thereby inhibiting colorectal cancer cell proliferation and migration, and suppressing the initiation and progression of colorectal cancer. These results expand the understanding of the regulatory mechanisms by which PAL influences colorectal cancer development, and may provide new potential targets for colorectal cancer diagnosis and therapy.