Abstract
Papillary thyroid carcinoma (PTC) is the most common type of thyroid cancer. Hydroxysteroid dehydrogenase like 2 (HSDL2) can regulate lipid metabolism and take part in cell proliferation. The purpose of the present study was to explore functional role of HSDL2 gene in PTC. The expression of HSDL2 protein in PTC tissues was estimated using immunohistochemistry analysis (IHC). HSDL2 mRNA level was detected through quantitative real-time polymerase chain reaction (qRT-PCR). Effects of HSDL2 gene on cell proliferation and apoptosis were assessed using the shRNA method for both in vitro and in vivo experiments. Potential target genes of HSDL2 were determined via bioinformatics analyses and Western blotting. HSDL2 was up-regulated in PTC tissues and cell lines compared with the controls (all P<0.05). Inhibiting HSDL expression could suppress PTC cell proliferation and cycle, and promote apoptosis in vitro. In vivo, the knockdown of HSDL2 gene could significantly suppress tumor growth (all P<0.05). Furthermore, AKT3, NFATc2 and PPP3CA genes might be potential targets of HSDL2 in PTC. HSDL2 expression was increased in PTC tissues and cells, which could promote tumor progression in vitro and in vivo.
Highlights
Papillary thyroid carcinoma (PTC) is the most common subtype of thyroid cancer
PTC tissues and adjacent normal ones were collected from 17 patients, who were pathologically diagnosed with PTC at Affiliated Hospital of the Academy of Military Medical Sciences
Numerous cancer-related genes have been identified to be closely correlated with PTC progression [24,25,26,27]
Summary
Papillary thyroid carcinoma (PTC) is the most common subtype of thyroid cancer. Its incidence exhibits continual increases in recent decades worldwide [1]. Diagnosis remains a great challenge in PTC, due to its asymptomatic nature at early stages. Fine needle aspiration biopsy (FNA) and ultrasound imaging are two commonly used methods for PTC diagnosis, which have relatively high accuracy [3,4]. Overall survival of PTC cases is significantly improved due to great advancements in therapeutic strategies, such as surgery, chemotherapy and radiotherapy [5]. The recurrence rate of PTC remains high, gravely weakening the effects of PTC treatment. This condition could partially be explained by increases in incurable cases and by limited understanding on the malignancy-related biological behaviors [6,7]. Exploring molecular mechanisms of PTC progression is critical to determine therapeutic targets for this malignant disease
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