Circular RNA_0000326 accelerates breast cancer development via modulation of the miR-9-3p/YAP1 axis.

Circular RNA (circ)_0000326 has been reported in bladder cancer and cervical cancer and is concerned to be involved with the development of cancerous cells. Whereas, there have been no reports concentrating on the influences of circ_0000326 in breast cancer (BC). Therefore, the latent modulatory mechanisms of circ_0000326 in BC are researched. circ_0000326 expression in BC tissues and correlative cells was evaluated via RT-qPCR, and the relevance between circ_0000326 expression and overall survival and the clinicopathological feature was also investigated. After a series of transfection, the effects of circ_0000326, microRNA-9-3p (miR-9-3p), and Yes-associated protein 1 (YAP1) in BC cell growth, invasion, and stemness were studied by CCK-8, flow cytometry, Transwell, and sphere-forming assays. The binding sites and correlation of circ_0000326, miR-9-3p, and YAP1 were certified via starBase website, luciferase reporter assay, and Pearson's χ2 test. The in vivo experiment was evaluated by establishing a subcutaneous tumorigenesis model. High-expressed circ_0000326 in BC tissues and cells was discovered, which was connected with an undesirable prognosis. Silencing of circ_0000326 visibly inhibited MCF-7 and BT549 cell growth, invasion, stemness, meanwhile declining the protein levels of SRY-related high-mobility group box gene 2 (SOX2) and octamer binding transcription factor 4 (OCT4). miR-9-3p was a sponger of circ_0000326, which was negatively regulated by circ_0000326. Moreover, YAP1 was confirmed as a target gene of miR-9-3p. circ_0000326 affected BC cell behaviors via mediating miR-9-3p and YAP1. Furthermore, circ_0000326 silencing prohibited tumor growth of BC in vivo. The research uncovered that circ_0000326 facilitated BC development via mediating the miR-9-3p/YAP1 axis.

[Study of a new zebrafish mutant defective in primitive myelopoiesis].

OBJECTIVE: To perform phenotypic identification and characteristic analysis of a new zebrafish mutant 1276 defective in primitive myelopoiesis. METHODS: The AB strain male zebrafish were mutagenized with N-ethyl N-nitrosourea (ENU) to induce mutations in the spermatogonial cells, and the mutations were transmitted to the offsprings. The F3 embryos were screened by neutral red staining for identifying the mutants defective in primitive myelopoiesis. One of the myeloid mutants 1276 was further studied by cytochemistry and whole mount in stiu hybridization (WISH) with different lineage markers. RESULTS: A total of 2140 mutagenized genomes from the 1296 F2 families were analyzed, and 12 mutants were identified to show abnormal signal by neutral red staining. In the primitive hematopoiesis stage, the mutant 1276 showed the absence of neutral red staining-positive cells in the whole body. The expression of microglia marker apoe was totally lost in the head of the mutant, and the expression of the macrophage marker l-plastin was slightly decreased in the head and remained normal in the ventral dorsal aorta region, but the granulocytes and erythrocytes developed normally. in the definitive hematopoiesis stage, the mutant 1276 still showed abnormal macrophages as found in the primitive hematopoiesis stage, but the granulocytes, erythrocytes and lymphocytes appeared normal. CONCLUSION: The zebrafish mutant 1276 shows abnormalities in the function, development and migration of the macrophages in the primitive hematopoiesis stage, which can not be compensated in the definitive hematopoiesis stage.