Considering the dilemma in papillary thyroid cancer treatment, this study intended to find solution in molecular respect. By probing into lncRNA-NEAT1/miR-129-5p/KLK7 interaction, this study would provide new targets for future treatment. Microarray analysis and R language package were applied to select possible lncRNA and miRNA. Luciferase reporter assay and RNA pull-down test were employed in the detection of target relationship between lncRNA and miRNA. Clone formation assay, flow cytometry analysis, wound healing assay, and transwell assay were, respectively, used to observe effects of lncRNA NEAT1/miR-129-5p/KLK7 to papillary thyroid cancer cells. Western blot and qRT-PCR were used to validate protein expressions and mRNA expressions in PTC tissues and cells. LncRNA NEAT1 was highly expressed in PTC tissues and cell lines and could deteriorate PTC by promoting proliferation, invasion, and migration accompanied by less apoptosis. Besides, miR-129-5p/lncRNA NEAT1 were found to negatively correlate with each other by direct target relationship and their combination suppressed the progression of PTC. KLK7, a highly expressed downstream protein in PTC tissues, could be directly regulated by miR-129-5p in a negative way. KLK7 accelerated the deterioration of PTC in vitro experiments which could be reversed by sh-lnc RNA NEAT1 and miR-129-5p mimics. In vivo experiments, silence of lncRNA NEAT1 restrain tumor growth in weight and volume. In conclusion, lncRNA NEAT1 suppression could inhibit PTC progression by upregulating miR-129-5p, which suppressed KLK7 expression either in vitro or vivo experiments.
Adrenomedullin is a 52-amino acid vasodilator peptide produced in many tissues, including bone. It has 20% sequence identity with amylin, a regulator of osteoblast growth, and circulates in picomolar concentrations. The present study assesses whether adrenomedullin also acts on osteoblasts. At concentrations of 10−12 M and greater, adrenomedullin produced a dose-dependent increase in cell number and [3H]thymidine incorporation in cultures of fetal rat osteoblasts. This effect was also seen with adrenomedullin-(15—52), -(22—52), and -(27—52), but adrenomedullin-(40—52) was inactive. These effects were lost in the presence of amylin blockers, suggesting they were mediated by the amylin receptor. Adrenomedullin also increased [3H]thymidine incorporation into cultured neonatal mouse calvaria but, unlike amylin, did not reduce bone resorption in this model. Adrenomedullin stimulated phenylalanine incorporation into both isolated osteoblasts and calvaria. When injected daily for 5 days over the calvariae of adult mice, it increased indexes of bone formation two- to threefold ( P < 0.0001) and increased mineralized bone area by 14% ( P = 0.004). It is concluded that adrenomedullin regulates osteoblast function and that it increases bone mass in vivo. The potential of this family of peptides in the therapy of osteoporosis should be further evaluated.
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