CircFOXM1 silencing represses cell proliferation, migration and invasion by regulating miR-515-5p/ADAM10 axis in prostate cancer.

Circular FOXM1 (circFOXM1) has been demonstrated to participate in the initiation and development of cancers, including prostate cancer (PCa). However, there is no relevant information on the regulation of PCa by circFOXM1. The RNA level of circFOXM1 was detected by qRT-PCR in PCa tissues and cells. The protein expression was performed by western blot and immunohistochemistry assay. Cell proliferation was examined by 3-(4,5)-dimethylthiahiazo (-z-y1)-3,5-di-phenytetrazoliumromide, colony formation and flow cytometry assays. The abilities of cell migration and invasion were determined by transwell assay. The relationship between circFOXM1 and miR-515-5p or ADAM10 was predicted by starBaseV2.0 online database, and identified by dual-luciferase reporter assay or RNA pull-down assay. The effects of circFOXM1 silencing and ADAM10 knockdown on PCa growth in vivo were evaluated by in-vivo tumor formation assay. As a result, we found that circFOXM1 and ADAM10 expression were upregulated in PCa tissues and cells. Functional analysis showed that circFOXM1 silencing repressed proliferation, migration and invasion, and induced cell cycle arrest, whereas these effects were partly reversed by miR-515-5p inhibitor. Additionally, circFOXM1 directly sponged miR-515-5p, and miR-515-5p bound to ADAM10. ADAM10 absence also repressed PCa process. Furthermore, in-vivo tumor formation assay revealed that both circFOXM1 silencing and ADAM10 knockdown repressed tumor growth in vivo. Thus, we came a conclusion that circFOXM1 contributed to PCa progression via regulating miR-515-5p/ADAM10 axis. These results may provide a theoretical basis for further studying the progression of PCa.

Liu GX ，Zheng T ，Zhang Y ，Hao P ... -  《-》

Effect of circFOXM1/miR-218-5p on the proliferation, apoptosis and migration of glioma cells.

Deng R ，Chen J ，Qin J ，Wang L ，Zhu D ，Sun X ... -  《-》

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

Fan X ，Liu M ，Fei L ，Huang Z ，Yan Y ... -  《-》

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

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.

Wang G ，Jiang Y ，Lu C ，Jiang W ，Wu S ，Hua Y ... -  《Scientific Reports》

LncRNA SNHG20 promotes cell proliferation and invasion via miR-140-5p-ADAM10 axis in cervical cancer.

Recent studies highlight the crucial regulatory roles of long non-coding RNAs (lncRNAs) in carcinogenesis. However, involvement of the lncRNA SNHG20 in cervical cancer progression remains unclear. The expression of SNHG20 and miR-140-5p was determined in cervical cancer. Gain or loss of function assays were used to explore the roles of SNHG20 and miR-140-5p in cervical cancer cells. Luciferase assay and Western blot were used to explore the underlying mechanisms of SNHG20 and miR-140-5p in cervical cancer progression. QRT-PCR showed that SNHG20 expression was significantly increased in cervical cancer. MiR-140-5p acted as a downstream target of SNHG20. SNHG20 inhibition or miR-140-5p overexpression reduced cervical cancer cells proliferation and invasion ability. Furthermore, we identified that ADAM10 could act as a potential target of miR-140-5p. MEK/ERK signaling could be inhibited by miR-140-5p mimics in cervical cancer cells. In addition, ADAM10 overexpression abrogated the effect of miR-140-5p mimics on cervical cancer cells proliferation and invasion. Our study demonstrated that SNHG20 could function as an oncogenic lncRNA by regulating miR-140-5p-ADAM10 axis and MEK/ERK signaling pathway in cervical cancer.

Guo H ，Yang S ，Li S ，Yan M ，Li L ，Zhang H ... -  《-》