Long noncoding RNA SNHG14 promotes malignancy of prostate cancer by regulating with miR-5590-3p/YY1 axis.

OBJECTIVE: Studies have demonstrated that long non-coding RNAs (lncRNAs) are important in the development and prognosis of prostate cancer. The aim of this study was to investigate the functions and mechanism of lnc-SNHG14 in prostate cancer. PATIENTS AND METHODS: Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) or Western blot (WB) were performed to detect mRNA expressions of SNHG14 and miR-5590-3p, and the protein levels of Yin Yang-1 (YY1) in prostate cancer tissues, adjacent tissues, and cancer cell lines. The correlation analysis was used to analyze the correlations between SNHG14, miR-5590-3p, and YY1. Kaplan-Meier survival analysis was used to analyze the overall survival for prostate cancer patients. Cell Counting Kit-8 (CCK-8) assay was performed to measure cell proliferation ability and flow cytometry assay was used to detect cell apoptotic rate. Besides, transwell assay was used to measure cell invasion ability. In addition, WB was performed to measure protein expressions in prostate cancer cell lines. Finally, Luciferase reporter assay was performed to verify the binding sites between SNHG14 and miR-5590-3p, miR-5590-3p, and YY1. RESULTS: The results showed that SNHG14 was significantly increased in prostate cancer tissues and prostate cancer cell lines, which were related with advanced stage and poor diagnosis for prostate cancer patients. MiR-5590-3p was reduced in prostate cancer tissues and cell lines, which were negatively correlated with SNHG14. YY1 was found to be increased in prostate cancer tissues, which was negatively correlated with miR-5590-3p and positively correlated with SNHG14. Furthermore, SNHG14 knockdown inhibited cell proliferation, invasion, and promoted cell apoptosis in DU145 cells. In addition, protein expressions of Cyclin D1, Bcl-2, and N-cadherin were repressed, and the levels of Bax, Cleaved Caspase-3, and E-cadherin were increased. Besides, miR-5590-3p inhibition promoted cell proliferation and invasion, and inhibited apoptosis in DU145 cells. Importantly, Luciferase reporter assay proved that SNHG14 could directly sponge with miR-5590-3p, which could bind with YY1 and regulate the functions of cancer cell. Finally, we proved that SNHG14 regulated cell proliferation, cell apoptosis, and invasion via miR-5590-3p/ YY1 axis in prostate cancer. CONCLUSIONS: Above all, we found that SNHG14 was increased in prostate cancer patients, which was related with future diagnosis for prostate cancer patients. Of note, we discovered that SNHG14 could promote cell proliferation, invasion, and repress cell apoptosis via miR-5590-3p/YY1 axis in prostate cancer, which might provide a new target for treating prostate cancer.

Hypercalcemia and status epilepticus relates to salmon calcitonin administration in breast cancer.

Calcitonin is currently used to treat hypercalcemia of many clinical types. However, we encountered a woman who suffered severe hypercalcemia and status epilepticus, both of which developed 8 days after the administration of salmon calcitonin for the treatment of breast cancer. When the patient first presented her serum calcium level was 15.5mg/dl, intact parathyroid hormone level 118 pg/ml, calcitonin <2 pg/ml, magnesium 1.2mg/dl, and phosphate 1mg/dl. Her serum calcium level returned to the reference range within 48 h after correction. At follow-up no hypercalcemia had developed, although the patient had received no further treatment for her breast cancer and multiple metastases were subsequently detected. Her hypercalcemia is ascribed to exogenous calcitonin supplementation. These conflicting events may be due to functionally heterogeneous calcitonin receptors or to activation of 1 alpha-hydroxylase by exogenous calcitonin.

[A preliminary study on the red cell immune function in blood stasis syndrome in traditional Chinese medicine].

20 patients with blood stasis syndrome (BSS), 20 patients with non-blood stasis syndrome (NBSS), and 17 normal subjects were measured by tests of RBC-C3b receptor rosette and RBC immune complex rosette. The rates of RBC-C3b receptor rosette formation (RBC-C3b RR, %) in BSS group, NBSS group and normal subjects were 20.90 +/- 4.02, 12.88 +/- 3.29 and 16.74 +/- 4.13 (P less than 0.01) respectively. The rates of RBC immune complex rosette formation (RBC-IC R, %) in the three groups were respectively 8.28 +/- 3.68, 7.73 +/- 2.48 and 7.41 +/- 2.43 (P less than 0.05). RBC-C3b RR was correlated to RBC-IC R in the normal subjects (r = 0.695, P less than 0.001). In patients with the same disease, RBC-C3b RR between the two syndromes (BSS and NBSS) was also very significantly different (P less than 0.01). This study suggested that there are variations on red cell immune function in BSS patients, and also provided an evidence that different syndromes of traditional Chinese medicine exist in diseases.