Abstract
The small nucleolar RNA host gene 12 (SNHG12) has been reported to play an important role in the tumorigenesis and progression of PCa, but the functional underlying mechanism has not been studied clearly. We detected the expression level of SNHG12 in PCa tissues and matched adjacent normal tissues that were collected from 85 patients. Then, colony formation assays, MTT experiments, and flow cytometry were used to examine the effect of SNHG12 on proliferation, cell cycle distribution, and apoptosis of DU145 cells. Further, Transwell invasion assay was utilized to assess whether SNHG12 participates in PCa cell invasion and affects the secretion of VEGF secretion in DU145 cells. Finally, we investigated the effect of SNHG12 on tumor growth in vivo. We found that SNHG12 promoted cell proliferation and suppressed apoptosis in PCa cells, which suggests that SNHG12 is probably a novel PCa biomarker and therapy target of PCa.
Highlights
Prostate cancer (PCa) is the second most frequent diagnosis male malignancies and the leading cause of death worldwide [1, 2]
We found that the expression of small nucleolar RNA host gene 12 (SNHG12) in PCa tissues was significantly higher than that in matched normal adjacent tissues (P < 0:05) (Figure 1(a))
We found that SNHG12 was significantly upregulated in the DU145 cell line compared with the normal human prostate stromal cell line (WPMY-1) and the other two human prostate carcinoma cell lines, LNCAP and PC-3 (Figure 1(b))
Summary
Prostate cancer (PCa) is the second most frequent diagnosis male malignancies and the leading cause of death worldwide [1, 2]. In China, PCa is one of the top ten leading causes of cancer-related death among men, and the morbidity and mortality rates of PCa are increasing annually rapidly, which is a serious risk to men’s life [3,4,5,6]. Further studying the mechanism underlying the pathogenesis and progression of PCa is very important and necessary. Changes in epigenetics have been increasingly recognized as important factors in the occurrence and development of PCa [9, 10]. The lncRNA CCAT1 promoted PCa cell proliferation by interacting with DDX5 and miR-28-5p [13]. High lncRNA FEZF1AS1 expression promoted cell proliferation and metastasis through Notch signaling in PCa [15]. Understanding the effects of lncRNAs on PCa could help identify novel diagnostic and therapeutic targets [16, 17]
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