Thyroid cancer is one of the most prevalent endocrine neoplasm. The present study examined the effects of Colorectal Neoplasia Differentially Expressed (CRNDE) on the progression of papillary thyroid cancer (PTC), and explored the underlying molecular mechanisms. Quantitative real-time PCR was used to detect CRNDE, miR-384 and pleiotrophin (PTN) mRNA expression. Western blot was used to measure PTN protein levels. Cell proliferation, cell growth, cell invasion and migration of PTC cells were determined by CCK-8, colony formation, transwell invasion and migration assays, respectively. CRNDE was up-regulated in PTC tissues and cell lines. Overexpression of CRNDE promoted BCPAP cell proliferation, invasion and migration, while knock-down of CRNDE suppressed K1 cell proliferation, invasion and migration. CRNDE negatively regulated the expression of miR-384 in PTC cells, which was further confirmed by luciferase reporter assay. MiR-384 was down-regulated and inversely correlated with CRNDE expression in PTC tissues. MiR-384 suppressed cell proliferation, invasion and migration in PTC cells, and enforced expression of miR-384 attenuated the oncogenic effects of CRNDE in PTC cells. PTN was predicted as a downstream target of miR-384, which was confirmed by luciferase reporter assay, and PTN was up-regulated in PTC tissues, and was negatively correlated with miR-384 expression and positively correlated with CRNDE expression in PTC tissues. In summary, our results suggested that the CRNDE/miR-384/PTN axis may play an important role in the regulation of PTC progression, which provides us with new insights into understanding the PTC.

Insecticides containing furan ring have attracted more attention owing to their unique mechanism of action. 25 furanone analogues were used to conduct a preliminary screening on insect cell line SL2 and these compounds exhibited good cytoactivity. Particularly, compound 14 presented good inhibitory effect with an IC 50 value of 28.14 μM. Subsequently, we investigated the selectivity against insect cells by testing the cytotoxicity of it on human cell line HEK293 and we noticed that compound 14 was less toxicity than the reference insect cells. Finally, we attempted to illustrate the act mechanism of compound 14 on SL2 cells at the cellular level and found it initiated apoptosis through a caspase-dependent mitochondrial pathway that down-regulated mitochondrial membrane potential level, increased the activity of caspase-3 and altered the cell cycle. The result showed that compound 14 could be considered as a new potent insecticide to be used for further optimization. ARTICLE HISTORY