Abstract
Previously, we found that the expression of long non-coding RNA (lncRNA) small nucleolar RNA host gene 17 (SNHG17) was up-regulated in castration-resistant prostate cancer (CRPC) cells compared to that in hormone sensitive prostate cancer (HSPC) cells. Moreover, we found that CD51 was up-regulated in prostate cancer cells and promoted the carcinogenesis and progression of prostate cancer. However, the regulatory mechanism of SNHG17 and CD51 in the development of CRPC remains unclear. In the current study, we aimed to elucidate the expressions, functions, and underlying mechanism of SNHG17 and CD51 in CRPC. Our results further confirmed that both SNHG17 and CD51 were up-regulated in CRPC tissues and cells. In addition, we found that SNHG17 expression was positively correlated with CD51 expression in prostate cancer. Mechanically, SNHG17 functioned as a competing endogenous RNA (ceRNA) to up-regulate CD51 expression through competitively sponging microRNA-144 (miR-144), and CD51 was identified as a direct downstream target of miR-144 in CRPC. Functionally, down-regulation of SNHG17 or up-regulation of miR-144 inhibited the proliferation, migration, and invasion of CRPC cells, whereas up-regulation of SNHG17 and down-regulation of miR-144 promoted the proliferation, migration and invasion of CRPC cells in vitro and in vivo. Using gain and loss-of function assay and rescue assay, we showed that miR-144 inhibited cell proliferation, migration and invasion by directly inhibiting CD51 expression, and SNHG17 promoted cell proliferation, migration and invasion by directly enhancing CD51 expression in CRPC cells. Taken together, our study reveals the role of the SNHG17/miR-144/CD51 axis in accelerating CRPC cell proliferation and invasion, and suggests that SNHG17 may serve as a novel therapeutic target for CRPC.
Highlights
It is estimated that there will be 174,650 newly diagnosed prostate cancer cases and 31,620 estimated prostate cancer related deaths in 2019 in the United States, accompanied by drastically increased incidence and mortality in China in the last decade (Chen et al, 2017; Siegel et al, 2019)
We found that the expression of small nucleolar RNA host gene 17 (SNHG17) was upregulated in the castration-resistant prostate cancer (CRPC) cell line C4-2 compared to hormone sensitive prostate cancer (HSPC) cell line LNCaP (Wang et al, 2014)
By generating comparative long non-coding RNA (lncRNA) profiles in the CRPC cell line C4-2 and the HSPC cell line LNCaP, we found that the expression of Linc00963 was upregulated in CRPC cells compared to that in HSPC cells (Wang et al, 2014)
Summary
It is estimated that there will be 174,650 newly diagnosed prostate cancer cases and 31,620 estimated prostate cancer related deaths in 2019 in the United States, accompanied by drastically increased incidence and mortality in China in the last decade (Chen et al, 2017; Siegel et al, 2019). Despite continuous improvements in diagnosis and treatment, the recommended maintenance schedules from androgen deprivation therapy (ADT) to radical resection are at present only effective in patients with hormonesensitive prostate cancer (HSPC) (Rice et al, 2019). This is when the tumor has progressed to castration-resistant prostate cancer (CRPC) stage, and the 5 years overall survival rate remains extremely disappointed (Nuhn et al, 2019). LncRNA small nucleolar RNA host gene 15 (SNHG15) has been shown to play oncogenic roles in the progression of prostate cancer (Zhang Y. et al, 2019). The expressions SNHG17 in CRPC tissues and its function in CRPC progression have not been fully investigated
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