Rabbit Anti-Human LATS2 (internal) Polyclonal antibody

Salivary glands, such as submandibular glands (SMGs), are composed of branched epithelial ductal networks that terminate in acini that together produce, transport and secrete saliva. Here, we show that the transcriptional regulator Yap, a key effector of the Hippo pathway, is required for the proper patterning and morphogenesis of SMG epithelium. Epithelial deletion of Yap in developing SMGs results in the loss of ductal structures, arising from reduced expression of the EGF family member Epiregulin, which we show is required for the expansion of Krt5/Krt14-positive ductal progenitors. We further show that epithelial deletion of the Lats1 and Lats2 genes, which encode kinases that restrict nuclear Yap localization, results in morphogenesis defects accompanied by an expansion of Krt5/Krt14-positive cells. Collectively, our data indicate that Yap induced Epiregulin signaling promotes the identity of SMG ductal progenitors and that removal of nuclear Yap by Lats1/2-mediated signaling is critical for proper ductal maturation.

This study aimed to evaluate the effects of miR-93 on the growth and invasiveness of prostate cancer (PC) cells (PCCs). Real-time PCR was carried out to detect the expression of miR-93 in the PC tissues and cell lines. The adjacent normal tissues served as controls. For in vitro experiments, methyl thiazolyl tetrazolium, clone formation, tumor cell invasion assays, and western blot analysis (WBA) were performed to confirm the variations in the proliferation and invasiveness of PCCs, prior and subsequent to transfection with an miR-93 antisense oligonucleotide (ASO), which blocks miR-93 binding to its target. Furthermore, the effect of miR-93 on the proliferation of PCCs was examined. Finally, the expression levels of the target genes of miR-93 were determined by WBA. miR-93 expression was higher in PC tissues than in the adjacent normal tissues, and a reduction in the miR-93 level remarkably inhibited the proliferation and invasiveness of PCCs. Moreover, miR-93 enhanced the expression of its target genes TGFBR2, ITGB8, and LATS2. The results of this study suggest that miR-93 may promote the proliferation and invasion of PCCs by upregulating its target genes TGFBR2, ITGB8, and LATS2.