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Baicalein suppressed cervical cancer tumourogenesis by modulating circ_0007364/microRNA-665/tumor protein D52 Axis

By: Liu, X.
Contributor(s): Zhu, Jingfang.
Publisher: Mumbai Indian Journal of Pharmaceutical Science 2023Edition: Vol.85(3), May-Jun.Description: 591-602p.Subject(s): PHARMACEUTICSOnline resources: Click here In: Indian journal of pharmaceutical sciencesSummary: Baicalein has anti-tumor effect and participates in multi-channel regulation mechanism. However, the mechanism of baicalein action has not been fully clarified in cervical cancer. Tumor protein D52, circ_0007364 and microRNA-665 expression were determined by quantitative reverse transcriptionpolymerase chain reaction. Tumor protein D52 and apoptosis-related proteins were detected by Western blot. Cell proliferation was measured via methyl thiazolyl tetrazolium, 5-ethynyl-2'-deoxyuridine and colony formation assays. The associations among microRNA-655, circ_0007364 and tumor protein D52 were determined by dual luciferase report assay. Cell invasion and apoptosis were assessed by Transwell assay and flow cytometry. The function experiments were carried out in vivo and in vitro. Baicalein significantly decreased circ_0007364 and tumor protein D52 expression and increased microRNA-665 expression in cervical cancer cell samples. Circ_0007364 or tumor protein D52 introduction and microRNA-665 down regulation weakened the suppressive effects of baicalein in cervical cancer cells. Moreover, circ_0007364 functioned by binding to microRNA-665 to regulate tumor protein D52 and affect cellular process in cervical cancer. Our founding showed that baicalein inhibited cervical cancer cell growth via regulating circ_0007364/microRNA-665/tumor protein D52 axis, further understanding the anticancer mechanism of baicalein and contributing to find more effective anticancer drug components for cervical cancer.
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Baicalein has anti-tumor effect and participates in multi-channel regulation mechanism. However, the mechanism of baicalein action has not been fully clarified in cervical cancer. Tumor protein D52, circ_0007364 and microRNA-665 expression were determined by quantitative reverse transcriptionpolymerase chain reaction. Tumor protein D52 and apoptosis-related proteins were detected by Western blot. Cell proliferation was measured via methyl thiazolyl tetrazolium, 5-ethynyl-2'-deoxyuridine and colony formation assays. The associations among microRNA-655, circ_0007364 and tumor protein D52 were determined by dual luciferase report assay. Cell invasion and apoptosis were assessed by Transwell assay and flow cytometry. The function experiments were carried out in vivo and in vitro. Baicalein significantly decreased circ_0007364 and tumor protein D52 expression and increased microRNA-665 expression in cervical cancer cell samples. Circ_0007364 or tumor protein D52 introduction and microRNA-665 down regulation weakened the suppressive effects of baicalein in cervical cancer cells. Moreover, circ_0007364 functioned by binding to microRNA-665 to regulate tumor protein D52 and affect cellular process in cervical cancer. Our founding showed that baicalein inhibited cervical cancer cell growth via regulating circ_0007364/microRNA-665/tumor protein D52 axis, further understanding the anticancer mechanism of baicalein and contributing to find more effective anticancer drug components for cervical cancer.

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