Open Access

ARTICLE

MicroRNA-181a is elevated by 10-hydroxycamptothecin and represses lung carcinoma progression by downregulating FOXP1

by LI PAN¹, WENTING YI², DONGMIN LIANG¹, YULONG ZHAO¹, RANRAN WANG¹, PINGYU WANG¹, YOUJIE LI¹, JIAXUAN XIN¹, YUNFEI YAN^1,#,*, SHUYANG XIE^1,#,*

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.

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