Abstract
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.
Highlights
Thyroid cancer is one of the most prevalent endocrine neoplasm with new cases of ~300,000 worldwide, and the median age at diagnosis for thyroid cancer is ~50 years old and the annual death is ~40,000[1]
To confirm the expression of Colorectal Neoplasia Differentially Expressed (CRNDE) in papillary thyroid cancer (PTC) tissues, we performed quantitative real-time PCR (qRT-PCR) experiments to determine the expression of CRNDE in 40 adjacent normal thyroid tissues and 40 PTC tissues, and CRNDE in the PTC tissues was up-regulated compared with adjacent normal tissues (Figure 1A)
Further mechanistic studies highlighted the important roles of CRNDE/miR-384/PTN axis in the progression of PTC, in which CRNDE promotes cell proliferation, invasion and migration at least partly via competitively binding miR384 in papillary thyroid cancer
Summary
Thyroid cancer is one of the most prevalent endocrine neoplasm with new cases of ~300,000 worldwide, and the median age at diagnosis for thyroid cancer is ~50 years old and the annual death is ~40,000[1]. Thyroid cancer is one of the most prevalent endocrine neoplasm with new cases of ~300,000 worldwide, and the median age at diagnosis for thyroid cancer is ~50 years old and the annual death is ~40,000. Papillary thyroid cancer (PTC) accounts for 80% of all thyroid cancers, and is the most common histological type [2]. The gold standard for diagnosis is needle aspiration biopsy, but the predicative value for recurrence is rather limited, due to the limited understanding of the mechanisms underlying PTC progression [4]. In this regard, investigating the molecular mechanism underlying PTC progression is extremely imperative and necessary
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