MiR-155 affects renal carcinoma cell proliferation, invasion and apoptosis through regulating GSK-3ß/ß-catenin signaling pathway.

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "MiR-155 affects renal carcinoma cell proliferation, invasion and apoptosis through regulating GSK-3ß/ß-catenin signaling pathway, by R.-J. Wei, C.-H. Zhang, W.-Z. Yang, published in Eur Rev Med Pharmacol Sci 2017; 21(22): 5034-5041-DOI: 10.26355/eurrev_201711_13813-PMID: 29228417" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/13813.

MiR-155 affects renal carcinoma cell proliferation, invasion and apoptosis through regulating GSK-3ß/ß-catenin signaling pathway.

OBJECTIVE: Glycogen Synthase Kinase-3ß (GSK-3ß) negatively regulates Wnt/ß-catenin signaling pathway through degrading ß-catenin protein. It plays an inhibitory role in various tumors, while the influence in the pathogenesis of renal carcinoma has not been elucidated. MicroRNA-155 (MiR-155) was found to be upregulated in renal carcinoma tissue. Bioinformatics analysis revealed the complementary binding site between miR-155 and 3'-UTR of GSK-3ß. This study investigated the influence of miR-155 in regulating GSK-3ß expression, Wnt/ß-catenin signaling pathway activity, and renal carcinoma cell proliferation, invasion, and apoptosis. PATIENTS AND METHODS: The targeted regulatory relationship between miR-155 and GSK-3ß were tested by dual luciferase assay. Renal carcinoma tissue and benign renal tissue were collected to detect miR-155 and GSK-3ß expressions. MiR-155, GSK-3ß, and ß-catenin levels were compared between HK-2 and 786-O cells. Renal carcinoma 786-O cells were cultured in vitro and divided into four groups, including miR-NC, anti-miR-155, pIRES2-blank, and pIRES2-GSK-3ß groups. Cell apoptosis was evaluated by flow cytometry. Cell invasion was determined by transwell assay. Cell proliferation was assessed by EdU staining. RESULTS: MiR-155 targeted regulated GSK-3ß expression. MiR-155 and ß-catenin expressions were significantly increased, while GSK-3ß level was significantly declined in renal carcinoma tissue compared with benign renal tissue. MiR-155 and ß-catenin expressions were significantly elevated, whereas GSK-3ß level was significantly downregulated in 786-O cells compared with HK-2 cells. Anti-miR-155 or pIRES2-GSK-3ß transfection significantly up-regulated GSK-3ß expression, attenuated ß-catenin level, restrained cell proliferation and invasion, and enhanced cell apoptosis. CONCLUSIONS: MiR-155 promoted renal carcinoma pathogenesis. Inhibition of miR-155 increased GSK-3ß expression, attenuated Wnt/ß-catenin signaling pathway, weakened proliferation and invasion, and facilitated apoptosis in renal carcinoma cells.

A study of CCND1 with epithelial ovarian cancer cell proliferation and apoptosis.

OBJECTIVE: Ovarian cancer is a gynecological malignancy with high mortality rates all over the world. Markers for diagnosis, prognosis and therapy are urgently required to improve the mortality rates. As a key proto-oncogene, CCND1 is known to be amplified in many different carcinomas, including breast cancer, esophageal cancer, bladder cancer, endometrial cancer and ovarian cancer, etc. CCND1 plays an important role in cancer development and progression. However, its function and mechanism have not been completely elucidated in ovarian cancer. MATERIALS AND METHODS: In the present study, we use cisplatin in vitro to inhibit the cell proliferation and promote cell apoptosis in epithelial ovarian cancer cell line SKOV-3. CCND1 expression, cell proliferation and cell cycle analysis were carried out by real-time PCR, CCK-8 and flow cytometry respectively. RESULTS: Our results demonstrated that cisplatin could inhibit the expression of CCND1 in human epithelial ovarian cancer cell line, which is related to the decreased cell proliferation and increased cell apoptosis. CONCLUSIONS: This study demonstrated that CCND1 is a potential therapeutic target for epithelial ovarian cancer treatment.

Serum levels of PSA, ALP, ICTP, and BSP in prostate cancer patients and the significance of ROC curve in the diagnosis of prostate cancer bone metastases.

Bone metastasis is a common complication in prostate cancer patients that can cause bone pain and pathological fracture. This study tested serum levels of prostate specific antigen (PSA), alkaline phosphatase (ALP), bone sialoprotein (BSP), collagen type I pyridine crosslinking peptide (ICTP) in prostate cancer patients and the significance of the receiver operator characteristic (ROC) curve in the diagnosis of prostate cancer bone metastases. Eighty-three prostate cancer patients were enrolled including 42 in the bone metastases group and 41 in the non-bone metastases group. Serum levels of BSP, ALP, ICTP, and PSA were highest in the bone metastases group followed by the non-bone metastases group, hyperplasia group, and then the control group (P < 0.05). Based on Gleason score, serum levels were highest in the poorly differentiated group followed by moderately differentiated and well-differentiated groups (P < 0.05). ROC curve analysis revealed that the diagnostic efficiency of the biomarkers in turn was BSP, PSA, ICTP, and ALP. The sensitivity of BSP, ALP, ICTP, and PSA in the diagnosis of prostate cancer bone metastases were 80.95, 57.14, 69.05, 71.43%, respectively, and the specificity of the same markers were 72.80, 64.80, 76.80, and 88.80%, respectively. Combined detection of the four markers improved sensitivity to 97.62% and the negative-predictive value increased to 97.60%. PSA + BSP showed the best efficiency when combining two markers. In conclusion, serum levels of BSP, ALP, ICTP, and PSA increased in patients with bone metastases, and combined detection of all markers could improve the positive-predictive value.

[Advance to the research of the climate factor effect on the distribution of plague].

Plague is an anthropozoonotic disease caused by the Yersinia pestis ,which developed by many factors including local climate factors. In recent years, more and more studies on the effects of climate on plague were conducted. According to the researches, climate factors (mainly the rainfall and temperature) affected the development and distribution of plague by influencing the abundance of plague host animals and fleas index. The climate also affected the epidemic dynamics and the scope of plague. There were significant differences existing in the influence of climate on the palgue developed in the north and south China. In the two different plague epidemic systems, the solitary Daurian ground squirrel-flea-plague and the social Mongolian gerbil-flea-plague, the obvious population differences existed among the responses of the host animal to the climate changes. Although the internal relationship between the rainfall, the flea index, the density of rodents and the plague supported the nutritional cascade hypothesis, it can not prove that there is a clear causality between the occurrence of plague and rainfall. So the influence of climate factors on plague distribution can only be used for early forecasting and warning of the plague.