RESUMEN
BACKGROUND: Prostate cancer is one of the malignant tumors of the urinary system and ranks second among the fatal cancers in men. And with age, the incidence of prostate cancer will increase linearly. METHODS: In this study, we measured the expression of Ubiquitin Conjugating Enzyme E2 V2 (UBE2V2) in prostate cancer tissues and cell lines by WB and explored the effect of UBE2V2 on the proliferation characteristics of prostate cancer by MTT and colony formation test. RESULTS: In our research, we found that the UBE2V2 protein level in prostate cancer cell lines was significantly higher than the UBE2V2 protein level in normal prostate cells, and the mRNA expression level did not change significantly compared with normal prostate tissue cells. At the same time, we found that miR-499a combined with UBE2V2 inhibited the expression of UBE2V2 in prostate cancer cells. CONCLUSIONS: In conclusion, our results indicate that miR-499a inhibits the proliferation of human prostate cancer cells by targeting UBE2V2, which will provide a potential target for the treatment of prostate cancer.
Asunto(s)
MicroARNs , Neoplasias de la Próstata , Apoptosis , Línea Celular Tumoral , Proliferación Celular , Regulación Neoplásica de la Expresión Génica , Humanos , Masculino , MicroARNs/genética , Pronóstico , Neoplasias de la Próstata/genéticaRESUMEN
Long non-coding RNA PSMG3-AS1 is known to play critical roles in several types of cancer, while its role in prostate carcinoma (PC) is unknown. This study aimed to explore the involvement of PSMG3-AS1 in PC. In this study, RT-qPCR analysis showed that PSMG3-AS1 was upregulated, while miR-106b was downregulated in PC. PSMG3-AS1 and miR-106b were inversely and significantly correlated across PC tissue samples. In addition, in PC cells, overexpression of PSMG3-AS1 increased the DNA methylation of miR-106b and decreased the expression levels of miR-106b. In contrast, no significant alteration in the expression of PSMG3-AS1 was observed in cells transfected with miR-106b mimic. Cell proliferation analysis showed that PSMG3-AS1 reduced the inhibitory effects of miR-106b overexpression on cell proliferation. Taken together, our data suggested that PSMG3-AS1 could downregulate miR-106b through DNA methylation to suppress PC cell proliferation.
Asunto(s)
Carcinoma , MicroARNs , ARN Largo no Codificante , Masculino , Humanos , MicroARNs/genética , ARN Largo no Codificante/genética , ARN Largo no Codificante/metabolismo , Metilación de ADN , Próstata/metabolismo , Proliferación Celular , Carcinoma/genética , Carcinoma/metabolismoRESUMEN
Prostate cancer (PC) is the most common type of newly diagnosed malignancy in men. Combined chemotherapy has been shown to be an effective strategy for the treatment of PC therapy. Lipid-polymer hybrid nanoparticles (LPNs) are core-shell nanoparticles composed of a polymer core and a lipid shell, which are reported to provide significant advantages for combined PC therapy. This study synthesized an aptamer conjugated ligand and designed an aptamer-functionalized, curcumin (CUR) and cabazitaxel (CTX) co-delivered LPNs (APT-CUR/CTX-LPNs). APT-CUR/CTX-LPNs had a mean size of 121.3 ± 4.2 nm and a positive surface charge (23.5 ± 2.6 mV). Both CUR and CTX were sustained released from LPNs. Aptamer-functionalized APT-CUR/CTX-LPNs exhibited good cell inhibition ability, high tumor accumulation, and remarkable tumor inhibition efficiency at the drug ratio of 2:5 (CUR:CTX). The novel LPNs offers great promise for the double drugs delivery to the prostate cancer cells and tumor xenograft in vivo, showing the potential of synergistic combination therapy for prostate cancer.