Down-regulated HSDL2 expression suppresses cell proliferation and promotes apoptosis in papillary thyroid carcinoma

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.

Knockdown of HSDL2 inhibits lung adenocarcinoma progression via down-regulating AKT2 expression

“…The cell cycle assay showed that siHSDL2 could block the progression of H1299 cells from S phase to G 2 /M phase and arrest the cell cycle in S phase, which caused mitotic arrest and apoptosis. This result is consistent with that from the study by Zeng et al [20], and also agrees with the results from our proliferation assay and apoptosis assay which showed that siHSDL2 inhibited the proliferation and promoted apoptosis of H1299 cells. Results from in vitro experiments disclosed that HSDL2 KD inhibited the growth and metastasis of lung adenocarcinoma.…”

“…Results from in vitro experiments disclosed that HSDL2 KD inhibited the growth and metastasis of lung adenocarcinoma. Several previous studies investigating the effects of HSDL2 in other malignant tumors have also confirmed the anti-tumor effects of HSDL2 KD [20][21][22][23]. But unfortunately, the molecular mechanism underlying the role of HSDL2 on tumor progression has not been further explored in these studies.…”

“…Studies have shown that the role of HSDL2 in tumor progression is complex and influenced by the type of tumor. HSDL2 has promoting effects on tumor progression in papillary thyroid cancer [20], bladder cancer [21], ovarian cancer [22], and glioma [23], but has suppressing effects in cholangiocarcinoma [24]. At present, the role of HSDL2 in the progression of NSCLC remains unclear.…”

HSDL2 Acts as a Promoter in Pancreatic Cancer by Regulating Cell Proliferation and Lipid Metabolism

“…These results were in agreement with the study of Zeng et al which showed that down-regulated HSDL2 expression suppresses cell proliferation and promotes apoptosis in papillary thyroid carcinoma. 20 Dong et al 21 reported that HSDL2 was strongly positive staining in breast cancer, and furthermore that knockdown of HSDL2 inhibited the proliferation and induced cell cycle arrest of breast cancer cells. Therefore we considered that HSDL2 may take part in the proliferation in PC cells and performed MTT, colony and EdU assays which confirmed this hypothesis.…”

Silibinin suppresses epithelial–mesenchymal transition in human non-small cell lung cancer cells by restraining RHBDD1

“…An IHC assay was conducted to evaluate the expression of RHBDD1 in FFPE NSCLC tissues and matched adjacent tissues using a previously described standard streptavidin-biotin-peroxidase complex method [30]. The samples were cut into 4-μm thick sections, which were deparaffinized in xylene and rehydrated in graded alcohol.…”