No abstract

Angiogenesis is essential for various biological processes, including tumor blood supply delivery, cancer cell growth, invasion and metastasis. Plasmacytoma variant translocation 1 (PVT1) long noncoding RNA (lncRNA) has been previously reported to affect angiogenesis of glioma microvascular endothelial cells by regulating microRNA (miR)‑186 expression level. However, the specific underlying molecular mechanism of PVT1 regulation of angiogenesis in vascular endothelial cells remains to be elucidated. The present study investigated the role of PVT1 in cell proliferation, migration and vascular tube formation of human umbilical vein endothelial cells (HUVECs) using MTT assay, Transwell migration assay and in vitro vascular tube formation assay, respectively. In order to determine the effect of miR‑26b on cell proliferation, migration and vascular tube formation of HUVECs, miR‑26 mimic or miR‑26b inhibitor were transfected into HUVECs. Reverse transcription‑quantitative polymerase chain reaction and western blotting were conducted to quantify the mRNA and protein expression levels of target genes. The present study confirmed that miR‑26b bound 3'‑untranslated region (3'‑UTR) and subsequently influenced gene expression level using dual luciferase reporter assay. The current study observed that PVT1 affected cell proliferation, migration and in vitro vascular tube formation of HUVECs. In addition, it was determined that PVT1 was able to bind and degrade miR‑26b to promote connective tissue growth factor (CTGF) and angiopoietin 2 (ANGPT2) expression. miR‑26b was also identified to have a suppressive role in cell proliferation, migration and in vitro vascular tube formation of HUVECs via binding 3'‑UTR regions and downregulating CTGF and ANGPT2 expression levels. The current findings may improve the understanding of the underlying mechanism of PVT1 contributing to angiogenesis of vascular endothelial cells and offer rationale for targeting PVT1 to treat angiogenesis dysfunction‑associated diseases, including cancer metastasis.

Background:The combination of partial absence of the sacrum, anorectal anomalies, and presacral mass constitutes Currarino syndrome (CS), which is associated with mutations in HLXB9. Methods: We analyzed 5 CS families and 6 sporadic cases for HLXB9 mutations by direct sequencing. Potentially pathologic expansions of HLXB9 GCC repeats were analyzed in patients, 4 general populations [Chinese, Japanese, Yoruba, and Centre du Etude Polymorphisme Human (CEPH)] from the HapMap project, and 145 healthy Chinese. Results: We identified 6 novel mutations affecting highly conserved residues (Ser185X, Trp215X, Ala26fs, Ala75fs, Met1Ile, and Arg273Cys). GCC allele and genotype distributions showed marked statistically significant differences. (GCC) 11 was the most common allele

During the development of human anorectum, it was intriguing to reveal that the URS never fused with the dorsal CM before dorsal CM disintegration, the normal anorectal development may depend on the dorsal cloaca and the dorsal CM; furthermore, the distribution of apoptosis and proliferation in the anorectum and ventral cloacal mesenchyme played a pivotal role in the formation of the anorectum.