Knockdown of long noncoding RNA linc-ITGB1 suppresses migration, invasion of hepatocellular carcinoma via regulating ZEB1.

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, "Knockdown of long noncoding RNA linc-ITGB1 suppresses migration, invasion of hepatocellular carcinoma via regulating ZEB1, by W.-W. Yu, K. Wang, G.-J. Liao, published in Eur Rev Med Pharmacol Sci 2017; 21 (22): 5089-5095-DOI: 10.26355/eurrev_201711_13823 -PMID: 29228420" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/13823.

LncRNA NKILA inhibits invasion and migration of osteosarcoma cells via NF-κB/Snail signaling pathway.

OBJECTIVE: Our research explored the possible biological function of long non-coding RNA (lncRNA) NKILA in the pathogenesis of osteosarcoma and its underlying mechanism. PATIENTS AND METHODS: NKILA expression in 60 cases of osteosarcoma and adjacent tissues was detected. The correlation between NKILA expression and clinical information was analyzed by Chi-square test. The overexpression plasmid or siRNA of NKILA were transfected into osteosarcoma cells by liposome. Cell proliferation was detected by cell counting kit-8 (CCK-8) assay. Transwell assay was used to check the migratory and invasive abilities. Western Blot was used to detect the expressions of nuclear factor-κB (NF-κB)-related proteins. In addition, we analyzed the cell invasion and migration after treatment of NF-κB inhibitor (JSH) to further verify whether NKILA can participate in the occurrence of osteosarcoma through the NF-κB / Snail signaling pathway. RESULTS: The expression level of NKILA in osteosarcoma tissues was significantly lower than that in adjacent tissues, and was related to tumor size, Enneking stage, and metastasis. After KNKS/NP cells were transfected with NKILA-siRNA, cell proliferation, invasion and migration were enhanced. Transfection of the NKILA overexpression plasmid in Saos2 cells reduced cell proliferation, invasion and migration. NKILA knockdown downregulated the expressions of p65 and E-cadherin, but strikingly increased Snail expression. The RNA binding protein co-immunoprecipitation experiments illustrated that p65 could bind to NKILA. Additionally, JSH was found to reverse the inhibitory effect of NKILA on cell migration and proliferation. CONCLUSIONS: NKILA was lowly expressed in osteosarcoma tissues. In addition, high expression of NKILA could suppress the migration and invasion of osteosarcoma cells by inhibiting the NF-κB/Snail signaling pathway.

Knockdown of long noncoding RNA linc-ITGB1 suppresses migration, invasion of hepatocellular carcinoma via regulating ZEB1.

OBJECTIVE: This research focuses on the influence of linc-ITGB1 on the metastasis of hepatocellular carcinoma and further explores its underlying mechanism. PATIENTS AND METHODS: A total of 70 hepatocellular carcinoma patients were chosen for our study. RT-qPCR was used for detecting the expression level of linc-ITGB1 in their cancer tissues. Moreover, the expression level of linc-ITGB1 was also detected in hepatocellular carcinoma cell lines. Furthermore, whether linc-ITGB1 could affect the migrated and invaded ability of hepatocellular carcinoma cells was determined by wound healing assay and transwell assay. We further explored the potential mechanism by RT-qPCR and Western blot assay. RESULTS: Linc-ITGB1 expression level in hepatocellular carcinoma tissues was remarkably higher than that in adjacent tissues. Moreover, migrated and invaded ability of hepatocellular carcinoma cells was inhibited through knockdown of linc-ITGB1. Further study revealed that silenced linc-ITGB1 inhibited the expression of ZEB1 and then suppressed epithelial to mesenchymal transition (EMT), which was important during the metastasis of hepatocellular carcinoma. Moreover, the inhibition of cell invasion by silenced linc-ITGB1 could be rescued through overexpression of ZEB1 in hepatocellular carcinoma. CONCLUSIONS: The results indicate that linc-ITGB1, a novel oncogene in tumorigenesis, could promote the metastasis and EMT via ZEB1, which may offer a possible therapeutic target in hepatocellular carcinoma.

Mechanism of age-related changes of bone marrow mesenchymal stem cells in senile osteoporosis.

This study was carried out to explore the age-related changes of bone marrow mesenchymal stem cells (BMMSCs) in mice as well as the influence of autophagy on the age-related changes of BMMSCs. BMMSCs aging-associated protein acetylation P53, P21 and P16 expressions in young and senile mice, protein expression of telomerase reverse transcriptase (TERT) as well as reactive oxygen species (ROS) level were detected and compared; the expression of BMMSCs autophagy associated gene, autophagy related protein molecule and LC3 molecule were detected; the influence of differently concentrated rapamycin and 3-MA on BMMSCs autophagy level was observed to select effective concentrations; the influence of rapamycin and 3-MA on BMMSCs cell cycle-related gene expression, apoptosis related gene expression and ROS level were discussed. Results revealed that the senile BMMSCs group had higher acetylation P53, P21 and P16 expression and fluorescence intensity than the young group, but its TERT expression, Beclin1 and LC3 gene expression and fluorescence intensity were lower than the young group. Both rapamycin and 3-MA inhibited CyclinD1 (CCND1) and CyclinD2 (CCND2) expression. Rapamycin promoted the expression of apoptosis-related genes Caspase3 and Caspase8 in the senile group, while 3-MA inhibited them in both the young and senile groups. It can therefore be concluded that senile BMMSCs have multiple age-related changes, performing as decrease of osteogenic capability and multiplication capacity, increase of acetylation P53, P21 and P16 protein expression, apoptosis and ROS level as well as decrease of telomerase activity. Furthermore, the autophagy level in senile BMMSCs reduced compared with young cells; autophagy activation can decrease ROS level and autophagy suppression improves ROS level; and autophagy regulation affects cell cycle and apoptosis.

Expression of TNF-α, VEGF, and MMP-3 mRNAs in synovial tissues and their roles in fibroblast-mediated osteogenesis in ankylosing spondylitis.

The aim of this study was to explore the mRNA levels of tumor necrosis factor-α (TNF-α), vessel endothelial growth factor (VEGF), and matrix metalloproteinase-3 (MMP-3) in synovial tissues in ankylosing spondylitis (AS), and to analyze the functions of these proteins in the differentiation of AS synovial tissue fibroblasts into osteoblasts (OB) and osteoclasts. Synovial tissue samples from 22 AS patients and 22 normal individuals were collected. In situ hybridization was utilized to detect TNF-α, VEGF, and MMP-3 transcripts. After counting numbers of positive cells, Spearman analysis was used to determine the correlation between transcriptional levels of the three mRNAs and the AS disease activity index (BASDAI) and the C-response protein (CRP) levels. With the addition of TNF-α, VEGF, or both factors into cultured normal synovial fibroblasts, osteocalcin (bone gla protein, BGP) secretion levels were compared. We found that expression of TNF-α, VEGF, and MMP-3 was identified exclusively in the disease group. mRNA levels were significantly positively correlated with BASDAI (r = 0.42, 0.38, and 0.47, respectively; P < 0.05) and CRP (r = 0.44, 0.34, and 0.47 respectively; P < 0.05) scores. The secretion level of BGP in normal synovial fibroblasts increased progressively with increasing concentrations of VEGF or TNF-α (P < 0.01 compared to levels before treatment). Furthermore, co-incubation using both VEGF and TNF-α significantly elevated BGP levels compared to the single addition of VEGF or TNF-α (P < 0.01). These results suggest TNF-α, VEGF, and MMP-3 might directly participate in the differentiation of fibroblasts into OBs.

Pathology of the annular ligament in paediatric Monteggia fractures.

OBJECTIVES: To report our operative findings regarding the annular ligament in paediatric Monteggia fractures and to propose treatment recommendation for Monteggia fracture. PATIENTS AND METHODS: A total of 35 children with type I and type III Monteggia fractures were treated operatively. The radial heads were all explored surgically in this series. The interposed ligament was stretched out of the joint space and was reduced around the radial head. In some of the patients, the joint capsule was repaired. Sixteen ulnar fractures were managed with open reduction and wire fixation, and 13 broken ulnas were fixed by plating. Six ulnar fractures were greenstick type and were treated by closed reduction and external fixation. RESULTS: All the patients were functionally excellent at the 6-month follow-up in terms of bone healing and the range of motion of the elbow joint. No redislocation or subluxation of the radial head was found until in the last follow-up. No heterotropic ossification was observed in any follow-up radiographs. CONCLUSIONS: The annular ligaments were intact in all paediatric patients with type I and type III Monteggia fractures and the ruptures were transversely on the joint capsule at the lower margin of the ligament. Most of the annular ligaments were interposed in the radiohumeral joint even though the radiographs showed reduction of the radial heads. We recommend reduction of the annular ligament in paediatric patients with Monteggia fractures.

Structure and expression of the D-amino-acid oxidase gene from the yeast Rhodosporidium toruloides.

D-Amino-acid oxidase (DAO2; EC 1.4.3.3) catalyses the oxidative deamination of D-amino acids to alpha-keto acids and ammonia. The purified DAO protein from Rhodosporidium toruloides was used to determine its amino acid sequence. Three internal peptide sequences, YCQYLARELQ, IAGIDDQAAEPIR and RCTMDSSDP, were obtained and used to synthesize four fully degenerated oligonucleotides for cloning of the DAO gene. Both cDNA and genomic DNA encoding R. toruloides DAO were cloned and sequenced. Comparison of these two DNA sequences revealed that the DAO gene contains six exons and five introns. The gene encodes a polypeptide of 368 amino acids with a calculated molecular mass of 40,079 Da. Using an Escherichia coli protein expression system, the DAO protein of R. toruloides can easily be produced in an active form and purified in a large quantity.