Open Access
ARTICLE
MicroRNA-181a is elevated by 10-hydroxycamptothecin and represses lung carcinoma progression by downregulating FOXP1
LI PAN1, WENTING YI2, DONGMIN LIANG1, YULONG ZHAO1, RANRAN WANG1, PINGYU WANG1, YOUJIE LI1, JIAXUAN XIN1, YUNFEI YAN1,*,#, SHUYANG XIE1,*,#
1 Department of Biochemistry and Molecular Biology, Binzhou Medical University, Yantai, 264003, China
2 Department of Medical Laboratory, Yantai Affiliated Hospital of Binzhou Medical University, Yantai, 264100, China
# These authors contributed equally to this work
* Corresponding Authors:SHUYANG XIE, ; YUNFEI YAN,
BIOCELL 2022, 46(2), 417-431. https://doi.org/10.32604/biocell.2022.015522
Received 05 January 2021; Accepted 30 March 2021; Issue published 20 October 2021
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
in vitro, 10-hydroxycamptothecin (10-HCPT) is
also capable of inhibiting angiogenesis
in vivo 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
in vitro 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.
Keywords
Cite This Article
PAN, L., YI, W., LIANG, D., ZHAO, Y., WANG, R. et al. (2022). MicroRNA-181a is elevated by 10-hydroxycamptothecin and represses lung carcinoma progression by downregulating FOXP1.
BIOCELL, 46(2), 417–431. https://doi.org/10.32604/biocell.2022.015522