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CircFOXM1 promotes proliferation and metastasis of hepatocellular carcinoma via regulating miR-1179/SPAG5 axis.

ABSTRACT: Hepatocellular carcinoma (HCC) predominantly occurs in patients with chronic liver disease, accounting for 70-90% of all liver cancer cases. The role of circFOXM1/miR-1179/SPAG5 axis in HCC has not been reported. This study aimed to explore the regulatory mechanism of circFOXM1 in HCC proliferation and metastasis. RNA polymerase inhibitor actinomycin D and RNase R exonuclease were used to identify circFOXM1 in HCC cells. The qRT-PCR was used to detect circFOXM1 expression. Specific siRNA for circFOXM1 was designed, and the sequence of circFOXM1 was inserted in pLCDH-ciR to overexpress circFOXM. Cell proliferation was detected by CCK8 in vitro, by tumor volume and tumor weight of HCC xenograft in vivo. Cell migration was detected by transwell test. Binding status of circFOXM1 with miR-1179 was detected by luciferase reporter gene assay. Rescue experiments were applied to identify the oncogenic mechanism of circFOXM1 in HCC cells. Actinomycin D assay confirmed the cyclization of circFOXM1. RNase R treatment showed that circFOXM1 was not affected by RNase R exonuclease. CCK8 assay, tumor volume and tumor weight showed that circFOXM1 effectively promoted HCC cell proliferation. Transwell assay showed that circFOXM effectively promoted migration and invasion abilities of HCC cells. Luciferase reporter gene activity assay showed that miR-1179 had complementary binding sites with circFOXM1 and SPAG5. CircFOXM1 silencing inhibited malignant phenotypes in HCC cells were partly rescued by either miR-1179 silencing or SPAG5 overexpression. CircFOXM1 promoted HCC cell proliferation and metastasis by regulating miR-1179/SPAG5 axis.

SUBMITTER: Wang G

PROVIDER: S-EPMC8668908 | biostudies-literature |

REPOSITORIES: biostudies-literature

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CircFOXM1 promotes the proliferation, migration, invasion, and glutaminolysis of glioblastoma by regulating the miR-577/E2F5 axis.

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Project description:Accumulating evidence indicates that circFOXM1 (Hsa_circ_0025033) is highly expressed in several cancers; however, the function of circFOXM1 in glioma and the molecular mechanism have not been well explored. In the present study, we found that expression of circFOXM1 was upregulated in both glioma tissues and cell lines. In addition, circFOXM1 knockdown suppressed glioma-cell proliferation, activated apoptosis in vitro, and repressed tumour growth in vivo. Moreover, we clarified that circFOXM1 binds with miR-432, which was downregulated in glioma cells. Furthermore, we indicated that Gα12, a direct target of miR-432, was highly expressed in glioma cells, and Gα12 silencing might limit the progression of glioma. Rescue assays indicated that Gα12 reversed the inhibitory effect of circFOXM1 silencing on glioma-cell tumorigenesis. In conclusion, circFOXM1 acts as a sponge of miR-432 to promote the proliferation and aggressiveness of glioma cells through the Gα12 signalling pathway.

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circFOXM1 contributes to sorafenib resistance of hepatocellular carcinoma cells by regulating MECP2 via miR-1324.

Project description:As one of the most common malignant tumors, hepatocellular carcinoma (HCC) is a leading cause of cancer-related deaths around the world. Emerging studies have indicated that circular RNAs (circRNAs), which play a crucial role in HCC pathogenesis and metastasis, are differentially expressed in HCC. However, the regulatory mechanisms of circRNA on sorafenib resistance of HCC are still unknown. In our study, we identified a novel circRNA, circFOXM1, using RNA sequencing (RNA-seq) that was increased in sorafenib-resistant HCC tissues. Functionally, circFOXM1 significantly inhibited HCC growth and enhanced sorafenib toxicity in vitro. Mechanistically, circFOXM1 acted as a sponge of microRNA (miR)-1324, which is a negative regulator of MECP2, indicating that circFOXM1 downregulation would regulate sorafenib resistance of HCC via releasing more free miR-1324 and suppressing MECP2 expression. Furthermore, miR-1324 overexpression was capable of reversing the circFOXM1-induced malignant phenotypes and elevated expression of MECP2 in HCC cells. circFOXM1 partially contributed to sorafenib resistance of HCC cells through upregulating MECP2 expression by sponging miR-1324.

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