@Article{or.2023.026959,
AUTHOR = {XIN LI, WENKAI JIANG, WANCHENG LI, SHI DONG, YAN DU, HUI ZHANG, WENCE ZHOU},
TITLE = {Betulinic acid-mediating miRNA-365 inhibited the progression of pancreatic cancer},
JOURNAL = {Oncology Research},
VOLUME = {31},
YEAR = {2023},
NUMBER = {4},
PAGES = {505--514},
URL = {http://www.techscience.com/or/v31n4/53314},
ISSN = {1555-3906},
ABSTRACT = { <b>Background:</b> The dilemma of pancreatic cancer treatment has become a global challenge. For this reason, effective, feasible, and new medical methods are currently much-needed. Betulinic acid (BA) has been valued as a potential therapy for pancreatic cancer. However, the mechanism by which BA exerts an inhibitory effect on the development of pancreatic cancer remains elusive. <b>Methods:</b> A rat model and two cell models of pancreatic cancer were established, and the effect of BA on pancreatic cancer was verified <i>in vivo</i> and <i>in vitro</i> by using MTT, Transwell, flow cytometry, RT-PCR, Elisa and immunohistochemistry. At the same time, miR-365 inhibitors were introduced to test whether BA played a role in mediating miR-365. <b>Results:</b> BA can significantly inhibit the proliferation and invasion of pancreatic cancer cells and promote apoptosis. <i>In vivo</i> experiments, BA can significantly lower the number of cancer cells and tumor volume in the rat model of pancreatic cancer. <i>In vitro</i>, it was found that BA inhibited the protein level and phosphorylation level of AKT/STAT3 by mediating the expression of miR365/BTG2/IL-6. Like BA, miR-365 inhibitors also significantly inhibited cell viability and invasion ability, and inhibited the protein level and phosphorylation level of AKT/STAT3 by changing the expression of BTG2/IL-6, and their combination had a synergistic effect. <b>Conclusion:</b> BA inhibits AKT/STAT3 expression and phosphorylation by modulating miR-365/BTG2/IL-6 expression, and BA inhibits the progression of pancreatic cancer through the aforementioned mechanism.},
DOI = {10.32604/or.2023.026959}
}