The circCDK17/miR-122-5p/ASF1B axis regulates the progression of cervical cancer.

BACKGROUND: Cervical cancer (CC) ranks fourth in terms of incidence and fourth in mortality overall in women worldwide. Circular RNAs (circRNAs) have been shown to be involved in the development of CC. However, the function of circRNA cyclin dependent kinase 17 (circCDK17, hsa_circ_0002762) in CC pathogenesis has not been studied. METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expression of related genes. MTT, thymidine analog 5-ethynyl-2'-deoxyuridine (EdU), flow cytometry, transwell and wound-healing assays were designed to analyze cell proliferation, cell cycle progression, migration and invasion, respectively. Western blot was utilized to examine the protein levels of Cyclin D1, E-cadherin and Vimentin. The relationship between miR-122-5p and circCDK17 or ASF1B was verified by dual-luciferase reporter assay. The xenograft model was established to study the role of circCDK17 in vivo. RESULTS: CircCDK17 and anti-silencing function 1B histone chaperone (ASF1B) were highly expressed in CC tissues and cells. Silencing circCDK17 reduced the proliferation, migration and invasion of CC cells. MiR-122-5p was a target of circCDK17. Silencing circCDK17 inhibited the malignant behaviors of CC cells by releasing miR-122-5p. Moreover, ASF1B was a target of miR-122-5p. Overexpression of ASF1B partially restored the inhibitory effects of circCDK17 silencing on cell proliferation, migration and invasion. Animal experiments confirmed the anti-tumor effect of circCDK17 knockdown in vivo. CONCLUSION: Our study demonstrates that circCDK17 regulates the expression of ASF1B by miR-122-5p competition and thus promotes the development of CC, providing a novel targeted therapy for CC.

[Effect of recombinant trichosanthin on proliferation of human cevical cancer Caski cells].

OBJECTIVE: To observe the effects of high expression of recombinant trichosanthin (rTCS) on the cell proliferation and cell cycle of human cervical cancer Caski cells. METHOD: Eukaryotic expression plasmid pcDNA3.1(-)/6His-TCS was constracted and stably transfected into Caski cells. RT-PCR,Western-blot were used to select the clones with rTCS high-expressing. Using pcDNA3.1(-)-transfected cells as the control, MTT assay and flowcytometry were used to elucidate the effects of rTCS high expression on cell growth and cycle regulation in Caski cells. RESULT: The Caski cells with stable high expression of rTCS was successfully established, which could inhibit the cell growth (P<0.01) and arrest Caski cells in G1 and G2 phases (P<0.05) obviously. CONCLUSION: High expression of rTCS can inhibit the growth of Caski cervical cancer cells, which might provide a new pathway for the therapy of cervical cancer.