@Article{biocell.2022.015522,
AUTHOR = {LI PAN, WENTING YI, DONGMIN LIANG, YULONG ZHAO, RANRAN WANG, PINGYU WANG, YOUJIE LI, JIAXUAN XIN, YUNFEI YAN, SHUYANG XIE},
TITLE = {MicroRNA-181a is elevated by 10-hydroxycamptothecin and represses lung carcinoma progression by downregulating FOXP1},
JOURNAL = {BIOCELL},
VOLUME = {46},
YEAR = {2022},
NUMBER = {2},
PAGES = {417--431},
URL = {http://www.techscience.com/biocell/v46n2/45100},
ISSN = {1667-5746},
ABSTRACT = {Tumor progression is usually characterized by proliferation, migration, and angiogenesis, which is essential for
supplying both nutrients and oxygen to the tumor cells. Therefore, targeting angiogenesis has been considered a
promising therapeutic strategy for cancer prevention and treatment. In the present study, we demonstrated that in
addition to suppressing lung cancer cell proliferation and migration <i>in vitro</i>, 10-hydroxycamptothecin (10-HCPT) is
also capable of inhibiting angiogenesis <i>in vivo </i>with a miR-181a-dependent manner. Mechanistically, by upregulating
miR-181a, which in turn downregulating FOXP1, 10-HCPT can inhibit the PI3K/Akt/ERK signaling pathwaymediated angiogenesis. Furthermore, reduced levels of miR-181a have been found in both lung cancer cell lines and
xenograft with concurrently elevated levels of FOXP1, VEGF, bFGF, and HDGF. Consistent with the findings from
the <i>in vitro</i> experiments, miR-181a impairs neovascularization in our xenograft model. In summary, our findings have
not only established the anti-oncogenic role of miR-181a in lung cancer angiogenesis but also suggest that 10-HCPT
could be a potential therapeutic reagent for lung cancer treatment.},
DOI = {10.32604/biocell.2022.015522}
}