Mechanism of LncRNA ROR promoting prostate cancer by regulating Akt.

We detected some serious inaccuracies and mistakes. Therefore, the article "Mechanism of LncRNA ROR promoting prostate cancer by regulating Akt, by X.-Q. Zhai, F.-M. Meng, S.-F. Hu, P. Sun, W. Xu, published in Eur Rev Med Pharmacol Sci 2019; 23 (5): 1969-1977-DOI: 10.26355/eurrev_201903_17235-PMID: 30915739" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/17235.

Mechanism of LncRNA ROR promoting prostate cancer by regulating Akt.

OBJECTIVE: To investigate the expression of long-chain non-coding RNA ROR in prostate cancer (PCa), and to further study its possible underlying mechanisms in prostate cancer. PATIENTS AND METHODS: Quantitative Real-time polymerase chain reaction (qRT-PCR) was performed to detect the level of lncRNA ROR in 42 pairs of PCa tissues and adjacent normal tissues, and the correlation between ROR level and PCa pathological parameters was also evaluated. Besides, ROR expression in PCa cells was further verified by qRT-PCR, and ROR knockdown model was constructed using lentivirus in PCa cell lines including PC-3 and Lncap. Cell counting kit-8 (CCK-8), transwell invasion and cell scratch assay were used to analyze the effect of ROR on the biological function of PCa cells and explore its underlying mechanism. RESULTS: QRT-PCR results demonstrated that ROR levels in PCa tissues were notably higher than that in normal ones, and the difference was statistically significant. Compared with patients with lowly-expressed ROR, patients with high ROR level had relatively more advanced tumor stage, higher incidence of lymph node or distant metastasis. Similarly, compared with negative control group, the cell proliferation, invasion and metastasis ability of the ROR knockdown group was significantly decreased. In addition, qRT-PCR results indicated that the expression of Akt, the key protein in the Akt signaling pathway, was significantly reduced in si-ROR cell lines. Furthermore, rescue experiment revealed that there was a mutual regulation between ROR and Akt. CONCLUSIONS: LncRNA ROR expression is strikingly increased in PCa tissues or cells, and is considerably associated with PCa stage, lymph node and distant metastasis. Additionally, LncRNA ROR may promote PCa cell proliferation, invasion and migration by regulating Akt.

High expression of lncRNA MEG3 participates in non-small cell lung cancer by regulating microRNA-7-5p.

OBJECTIVE: This study was made to investigate whether long noncoding RNA (lncRNA) MEG3 could participate in the occurrence and development of non-small cell lung cancer (NSCLC) by regulating the expression of BRCA1 through competitive binding to microRNA-7-5p. PATIENTS AND METHODS: We used quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) to explore the expression of lncRNA MEG3 and BRCA1 in NSCLC tissues and adjacent normal tissues, as well as NSCLC cell lines. The dual luciferase reporter gene assay was used to detect the binding of microRNA-7-5p to lncRNA MEG3 and BRCA1. Meanwhile, the expression of BRCA1, B-cell lymphoma-2 (Bcl-2) and BCL2-associated X (Bax) was detected by Western blot after the cells were overexpressed or knocked down of lncRNA MEG3. All these experiments were designed to investigate whether lncRNA MEG3 participated in the pathogenesis of NSCLC through inhibiting the expression of BRCA1 and Bcl-2 and promoting Bax expression. RESULTS: The expressions of lncRNA MEG3 and BRCA1 in NSCLC tissues and A549 and HCC823 cell lines were significantly lower than those in the normal group. Overexpression of lncRNA MEG3 and BRCA1 in A549 and HCC823 cell lines resulted in increased apoptosis of lung cancer cells. Dual luciferase reporter assay demonstrated that lncRNA MEG3 can regulate the expression of BRCA1 through competitively binding to microRNA-7-5p to form the lncRNA MEG3/microRNA-7-5p/BRCA1 regulatory network. Besides, lncRNA MEG3 could inhibit the apoptosis inhibitory protein Bcl-2 and promote the expression of apoptosis-promoting factor Bax. CONCLUSIONS: LncRNA MEG3 was significantly downregulated in NSCLC, and it could regulate the BRCA1 expression by competitive binding to microRNA-7-5p.

miR-564 inhibited metastasis and proliferation of prostate cancer by targeting MLLT3.

OBJECTIVE: MiR-564 has been discovered to be abnormally expressed in human malignancy. Two recent studies suggested that miR-564 plays a role in tumor inhibition in both lung and breast cancer. However, no evidence reported the mechanism and function of miR-564 in prostate cancer (PCa). PATIENTS AND METHODS: The PCa tissues and their adjacent normal tissues were collected from 50 PCa patients. Expressions of miR-564 in tissues and cells were evaluated with RT-qPCR. The MTT [3-(4,5-dimethylthiazol-2-yl)2,5-diphenyl tetrazolium bromide] assay, flow cytometry and Western-blot analysis, were applied to detect the proliferation, cell cycle progression and the protein expression of PCa cell lines (PC-3 and DU-145). Migration and invasion of PCa cells were analyzed by Transwell assays. Furthermore, the correlation between miR-564 and MLLT3 was assessed by luciferase reporter assay. Also, the PCa cells were transfected with miR-564 mimics control and inhibitor. RESULTS: In our present research, miR-564 was found dysregulated in PCa cells and to act as a suppressor in PCa cell proliferation, progression of cell cycle, cell invasion and migration. MLLT3 (also known as Af9) is a proto-oncogene, which has first reported in leukemia, and the regulation of its expression remains incompletely elucidated. Also, it is first reported in our study, suggesting that MLLT3 is a direct target of miR-564. The results also showed a significant negative correlation with miR-564 in PCa cells. Furthermore, up-regulation of MLLT3 attenuates the effects of miR-564 on the ability of PCa cells. CONCLUSIONS: Our research demonstrated the suppressor function of miR-564 in PCa, revealing restoration of miR-564 as a potential therapeutic strategy for the treatment of PCa.

MiR-576-3p is a novel marker correlated with poor clinical outcome in bladder cancer.

OBJECTIVE: MicroRNAs play important roles in the regulation of the initiation and progression of bladder cancer. To our best knowledge, the prognostic value of miR-576-3p in bladder cancer has not been reported. Thus, the purpose of the current study was to determine the expression of miR-576-3p and assess the clinical significance of miR-576-3p in bladder cancer. PATIENTS AND METHODS: Quantitative real-time polymerase chain reaction (RT-PCR) was performed to evaluate miR-576-3p levels in 232 pairs of bladder cancer specimens and adjacent noncancerous tissues. The association of miR-576-3p expression with clinicopathological factors was statistically analyzed. Overall survival was calculated and survival curves were plotted using the Kaplan-Meier method. The influence of each variable on survival was examined by the Cox multivariate regression analysis. RESULTS: Our data showed that the expression of miR-576-3p was significantly decreased in bladder cancer tissue compared with matched bladder tissues (p < 0.01). Low miR-576-3p expression level was significantly associated with advanced tumor stage (p = 0.004), lymph node metastasis (p = 0.027), and recurrence (p = 0.018). The results of Kaplan-Meier survival analysis showed that patients with low miR-576-3p expression presented shorter mean months of overall survival than patients with high miR-576-3p expression (p < 0.0001). Finally, the univariate and multivariate analysis showed that miR-576-3p expression was an independent prognostic marker of overall survival of bladder cancer patients. CONCLUSIONS: Our results demonstrated that down expression of miR-576-3p in bladder cancer was associated with an unfavorable prognosis, and miR-576-3p might be clinically applicable as an indicator of favorable prognosis.

Combined folate gene MTHFD and TC polymorphisms as maternal risk factors for Down syndrome in China.

We examined whether polymorphisms in the methylenetetrahydrofolate dehydrogenase (MTHFD) and transcobalamin (TC) genes, which are involved in folate metabolism, affect maternal risk for Down syndrome. We investigated 76 Down syndrome mothers and 115 control mothers from Bengbu, China. Genomic DNA was isolated from the peripheral lymphocytes. Polymerase chain reaction and restriction fragment length polymorphism were used to examine the polymorphisms of MTHFD G1958A and TC C776G. The frequencies of the polymorphic alleles were 24.3 and 19.1% for MTHFD 1958A, 53.9 and 54.2% for TC 776G, in the case and control groups, respectively. No significant differences were found between two groups in relation to either the allele or the genotype frequency for both polymorphisms. However, when gene-gene interactions between these two polymorphisms together with previous studied C677T and A1298C polymorphisms in the methylenetetrahydrofolate reductase (MTHFR) gene were analyzed, the combined MTHFR 677CT/TT and MTHFD 1958AA/GA genotype was found to be significantly associated with the risk of having a Down syndrome child [odds ratio (OR) = 3.11; 95% confidence interval (95%CI) = 1.07-9.02]. In addition, the combined TC 776CG and MTHFR 677TT genotype increased the risk of having a child with Down syndrome 3.64-fold (OR = 3.64; 95%CI = 1.28-10.31). In conclusion, neither MTHFD G1958A nor TC C776G polymorphisms are an independent risk factor for Down syndrome. However, the combined MTHFD/MTHFR, TC/MTHFR genotypes play a role in the risk of bearing a Down syndrome child in the Chinese population.

Identification of forensically important flesh flies based on a shorter fragment of the cytochrome oxidase subunit I gene in China.

With the development of molecular identification, there has been a great deal of discussion about the feature of the mitochondrial DNA (mtDNA) fragments. Although longer fragments may minimize stochastic variation across taxa and be more likely to reflect broader patterns of nucleotide divergence, shorter fragments have many advantages, such as quick, easy and economical. Extensive application of long mtDNA segments for species identification cannot always be achieved as a result of constraints in time and money. In the present study, a molecular identification method involving the sequencing of a 272-bp 'barcode' fragment of the mitochondrial cytochrome oxidase subunit I (COI) gene from 55 specimens, representing 7 Chinese sarcophagid species from varying populations, was evaluated. Phylogenetic analysis of the sequenced segments showed that all sarcophagid specimens were properly assigned into seven species, which indicated the possibility of separation congeneric species with the short fragments. The results of this research will be instrumental for the implementation of the Chinese Sarcophagidae database.

Mitochondrial DNA and STR analyses for human DNA from maggots crop contents: a forensic entomology case from central-southern China.

Insect larvae and adult insects found on human corpses can provide important forensic evidence however it is useful to be able to prove evidence of association. Without this, it could be claimed that the insect evidence was a contaminant or had been planted on the body. This paper describes how mitochondrial DNA (mtDNA) and STR analysis of the crop contents of larvae of the blowfly Aldrichina grahami collected from separated body parts was used to provide evidence of association.

Effect of sodium glycyrrhetinate on neonatal rat myocardial cells.

AIM: To investigate the effect of sodium glycyrrhetinate (SG) on neonatal rat myocardial cells. METHODS: The neonatal rat myocardial cells were cultured in vitro. Radioimmunoassay and fluorimetry were used to determine cAMP and [Ca2+], respectively. RESULTS: The beating rate of myocardial cells was depressed by SG 0.4 mmol.L-1 at 5, 10, and 15 min, from 73 +/- 9 min-1 to 62 +/- 5, 59 +/- 7, and 56 +/- 6 min-1, respectively. SG 0.1 and 0.2 mmol.L-1 showed above similar results at 15 min and 10, 15 min, respectively. When the myocardial cells were incubated with SG 0.2 and 0.4 mmol.L-1 at 37 degrees C for 10 and 15 min, the concentration of cAMP and- [Ca2+] were reduced. cAMP contents in SG 0.2 mmol.L-1 treated group at 10 and 15 min were lower than control group (1.09 +/- 0.18 vs 1.65 +/- 0.48 pmol per vial, P < 0.05; 1.12 +/- 0.35 vs 1.72 +/- 0.49 pmol per vial, P < 0.01), and so was [Ca2+] (30 +/- 4 nmol.L-1 vs 41 +/- 6 nmol.L-1, P < 0.05 and 28 +/- 6 nmol.L-1 vs 38 +/- 7 nmol.L-1, P < 0.01). SG 0.1 and 0.2 nmol.L-1 increased the pO2 change rate (87% +/- 5%, 75% +/- 4% vs 54% +/- 3%, P < 0.01) in suspension fluid of myocardial cells, but SG 0.4 mmol.L-1 decreased it (31% +/- 2% vs 54% +/- 3%, P < 0.01). CONCLUSION: SG protects myocardium or treats ischemic cardiac disease.