LncRNA SNHG1 promotes renal cell carcinoma progression through regulation of HMGA2 via sponging miR-103a.

BACKGROUND: Long noncoding RNAs (LncRNAs) plays a vital role in tumorigenesis and development. The molecular mechanism of SNHG1 in renal cell carcinoma (RCC) has not been illustrated. The aim of this research was to explore the expression and function of LncRNA SNHG1 in RCC. MATERIAL AND METHODS: The expression of SNHG1 in clinical tissues and RCC cell lines was detected. Luciferase reporter assay was performed to verify the correlation between SNHG1, miR-103a, and HMGA2. CCK-8 assay was performed to examine cell viability. Cell apoptosis was analyzed using flow cytometry. Cell invasion capacity was determined by Transwell assays. The protein level of HMGA2 was analyzed by Western blotting. RESULTS: The expression of SNHG1 markedly increased in RCC tissues and cell lines. Subsequent studies identified SNHG1 as a miRNA sponge for miR-103a. In addition, SNHG1 knockdown and miR-103a overexpression significantly inhibited progression of RCC. miR-103a also regulated HMGA2 levels. CONCLUSION: Our findings showed that SNHG1 was upregulated in RCC cells and tissues. SNHG1 promoted the malignant characteristics of RCC cells. Its regulatory effect may be regulation of HMGA2 by sponging miR-103a. Therefore, Our study facilitates the understanding of SNHG1 function in RCC.

miR­539 suppresses proliferation and induces apoptosis in renal cell carcinoma by targeting high mobility group A2.

Renal cell carcinoma (RCC) is one of the most common urinary malignancies with a high rate of morbidity. MicroRNAs (miRNAs) have been shown to be critical post­transcriptional regulators in tumorigenesis. The present study aimed to investigate the effect of miRNA (miR)­539 on the proliferation and apoptosis of RCC. The expression of miR­539 and high mobility group AT­hook 2(HMGA2) were examined in clinical RCC specimens. The 786­O RCC cell line was also used and was transfected with miR­539 mimics or inhibitors. The correlation between miR­539 and HMGA2 was confirmed using a luciferase reporter assay. Cell viability and apoptosis were detected using MTT and flow cytometry assays. The protein levels of HMGA2, AKT, phosphorylated (p)­AKT, mammalian target of rapamycin (mTOR) and p­mTOR were analyzed using western blot analysis. The results revealed that miR­539 was negatively correlated with the expression of HMGA2 in clinical RCC specimens. Further experiments identified HMGA2 as a direct target of miR­539. The overexpression of miR­539 downregulated the expression of HMGA2, reduced cell proliferation and promoted cell apoptosis, whereas the knockdown of miR­539 led to the opposite results. miR­539 also suppressed the phosphorylation of AKT and mTOR, without altering the levels of total AKT and mTOR. Taken together, the results of the present study indicated that miR­539 negatively regulated the expression of HMGA2 in clinical specimens and in vitro. miR539 inhibited cell proliferation and induced apoptosis in RCC cells. This regulatory effect of miR­539 may be associated with the AKT signaling pathway. Therefore, miR­539 may be used as a biomarker for predicting the progression of RCC.

[Oral Testosterone Undecanoate Capsules combined with Qilin Pills for late-onset hypogonadism in males].

OBJECTIVE: To investigate the clinical effects of oral Testosterone Undecanoate Capsules (TUC) combined with Qilin Pills (QLP) on late-onset hypogonadism (LOH) in men. METHODS: Sixty-three LOH patients meeting the inclusion criteria were randomly divided into a control group (aged ï¼»48.4 ± 6.2ï¼½ yr, n = 32) and an experimental group (aged ï¼»47.2 ± 5.6ï¼½ yr, n = 31) to be treated with oral TUC (80 mg, qd) and TUC + QLP (6g, tid), respectively, both for 3 months. Comparisons were made between the two groups of patients in the IIEF-5 scores, total testosterone (TT) levels, and scores in the Aging Males' Symptoms (AMS) scale before and after treatment. RESULTS: After treatment, the patients of the experimental group, as compared with the controls, showed a significantly increased IIEF-5 score (21.7 ± 5.8 vs 15.9 ± 4.7, P <0.05) and TT level (ï¼»16.7 ± 2.2ï¼½ vs ï¼»13.1 ± 2.8ï¼½ nmol/L, P <0.05), but a decreased AMS score (20.7 ± 5.7 vs 31.3±6.5, P <0.05). CONCLUSIONS: TUC combined with Qilin Pills has a better effect and a lower rate of adverse reactions than TUC used alone in the treatment of late-onset hypogonadism in males.