Retraction Note: LINC01296 promotes the proliferation and invasion by regulating microRNA-760 expression and predicts poor prognosis of hepatocellular carcinoma.

The article "LINC01296 promotes the proliferation and invasion by regulating microRNA-760 expression and predicts poor prognosis of hepatocellular carcinoma", by Z.-C. Wang, S. Yang, M.-Q. Chen, S.-S. Wu, H.-H. Lv, W.-X. Jin, published in Eur Rev Med Pharmacol Sci 2019; 23 (22): 9848-9856-DOI: 10.26355/eurrev_201911_19548- PMID: 31799652 has been retracted by the author for the following reasons: After the publication of this article, the authors reviewed the process of the experiment and found there were mistakes in the methodology search. Not all the carcinoma specimens used in the experiment were from hepatocellular carcinoma. The prognosis and clinical features the rate of lymph node metastasis and the treatment and prognosis between these types of cancers are different. For example, intrahepatic cholangiocarcinoma tends to involve a high frequency of lymph node metastasis, and the prognosis is worse than hepatocellular carcinoma; hepatocellular carcinoma seldom involves lymph node metastasis but often involves intrahepatic metastasis; colorectal cancer liver metastasis is far more sensitive to chemotherapy and has a relatively long survival, and neuroendocrine carcinoma is sometimes sensitive to hormone therapy and generally has better survival than hepatocellular carcinoma. As a result, the clinical results and gene test results mentioned in this article were incorrect. After that the authors found that there was a mistake, they subsequently carried out supplementary experiments and found that they could not confirm that there was an increase in the expression of the LICO01296 gene in hepatocellular carcinoma, so they could not link some clinical results with the results of the basic research results mentioned in this article. Therefore, from the perspective of academic rigor, they requested to withdraw the article. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/19548.

Correlation between carotid atherosclerotic plaque properties and serum levels of lncRNA CCAT2 and miRNA-216b.

OBJECTIVE: The purpose of this study was to uncover the clinical values of serum long non-coding RNA (lncRNA) CCAT2 and miRNA-216b in the properties of carotid atherosclerotic plaques. PATIENTS AND METHODS: Patients with carotid atherosclerotic plaques were assigned into stable plaque group (n=60) and unstable plaque (n=75) group based on their examination results of cervical contrast-enhanced CT examination. Maximal plaque thickness (MAPT) and intima-media thickness (IMT) in each group were determined. Serum levels of lncRNA CCAT2 and miRNA-216b in patients with carotid atherosclerotic plaques were detected by Reverse Transcriptase-Polymerase Chain Reaction (RT-PCR). Moreover, the correlation between serum levels of CCAT2 and miRNA-216b was analyzed by Pearson's correlation analysis. Besides, potential correlations of serum levels of CCAT2 and miRNA-216b with MAPT and IMT in patients with carotid atherosclerotic plaques were assessed as well. RESULTS: Results revealed that MAPT and IMT were markedly higher in unstable plaque group than those in stable plaque group. Serum level of CCAT2 was higher in unstable plaque group, while miRNA-216b was lower than those in stable group. A negative correlation was identified between serum levels of CCAT2 and miRNA-216b. In addition, CCAT2 level was positively correlated with IMT and MAPT in patients with carotid atherosclerotic plaques, while miRNA-216b level was negatively correlated with them. CONCLUSIONS: Detection of serum levels of CCAT2 and miRNA-216b could be applied for predicting the rupture of carotid atherosclerotic plaques. They may be potential biomarkers predicting ischemic stroke.

LINC01296 promotes the proliferation and invasion by regulating microRNA-760 expression and predicts poor prognosis of hepatocellular carcinoma.

OBJECTIVE: The aim of this study was to investigate the role of LINC01296 in the progression of liver cancer (LCa) and to explore its possible molecular mechanisms. PATIENTS AND METHODS: TCGA database was used for information mining to verify the expression of LINC01296 in liver tumor tissues and normal tissues. The levels of LINC01296 in 40 pairs of LCa and adjacent tissues, as well as normal liver cell lines and liver cancer cell lines, were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The Chi-square test was performed to analyze the clinical characteristics of tumor samples and LINC01296 expression. Meanwhile, the Chi-square test was used to explore the relationship between different clinical indicators and the expression of LINC01296. The liver cancer cell lines were screened and transfected with siRNA-LINC01296 and microRNA-760 inhibitor, as well as corresponding negative controls, respectively. Cell counting kit-8 (CCK-8) and Transwell assays were used to determine the effects of LINC01296 on the proliferative and invasive capacities of cells. Furthermore, the regulatory association between LINC01296 and microRNA-760 was verified by the Dual-Luciferase reporter assay. RESULTS: LINC01296 expression was remarkably higher in LCa tissues than that of normal liver tissues. Meanwhile, LINC01296 expression was associated with poor prognosis of LCa. Patients with high LINC01296 expression were more likely to have lymph node metastasis. In vitro experiments showed that the knockdown of LINC01296 significantly inhibited the proliferation and migration of HCC cells. Meanwhile, microRNA-760 was remarkably lowly expressed in LCa tissues and cells. Subsequent experiments indicated that LINC01296 was regulated by miR760 in LCa tissues, and high expression of linc0129 could limit microRNA-760 expression. Furthermore, the inhibition of microRNA-760 in HCC cells reversed the effect of LINC01296 knockdown on cell proliferation and invasion. CONCLUSIONS: LINC01296 could promote the proliferative ability and invasiveness of hepatoma cells by inhibiting the expression of microRNA-760. Moreover, its expression was closely related to lymph node metastasis and poor prognosis of LCa.

Effect of polymorphisms of vascular endothelial growth factor on prognosis in osteosarcoma patients.

We investigated the association between vascular endothelial growth factor (VEGF) gene +1612G/A, -634C/G, and +936G/C and the clinical outcome of osteosarcoma. Genomic DNA was isolated from blood samples, and 3 VEGF gene polymorphisms (+1612G/A, -634C/G, and +936G/C) were analyzed using polymerase chain reaction-restriction fragment length polymorphism. Of the 194 patients, 82 patients (42.27%) showed a good response to chemotherapy, while 73 (37.63%) died during the follow-up period. When comparing good and poor responders, we observed no significant association between the VEGF +1612G/A, -634G/C, and +936T/C polymorphisms and clinical outcome of osteosarcoma patients. According to Cox regression analysis, the VEGF +1612A/G, -634G/C, and +936T/C polymorphisms did not statistically significantly increase the risk of overall survival of patients with osteosarcoma. This study showed that VEGF +1612A/G, -634G/C, and +936T/C polymorphisms were not related to the response to chemotherapy and clinical outcome of osteosarcoma patients.

Expression of glutamine synthetase in Tegillarca granosa (Bivalvia, Arcidae) hemocytes stimulated by Vibrio parahaemolyticus and lipopolysaccharides.

The blood cockle, Tegillarca granosa, is a widely consumed clam in the Indo-Pacific region. Glutamine synthetase (GS) is an enzyme that plays an essential role in the metabolism of nitrogen by catalyzing the condensation of glutamate and ammonia to form glutamine. We identified the GS of T. granosa (Tg-GS) from hemocytes by 3'- and 5'-rapid amplification of cDNA ends (RACE)-PCR. The full-length cDNA consisted of 1762 bp, with a 1104-bp open reading frame encoding 367 amino acids. Sequence comparison showed that Tg-GS has homology to GS of other organisms, with 79.78% identity with GS from the Pacific oyster Crassostrea gigas, 71.98% identity with GS from the zebrafish Danio rerio, and 68.96% identity with human Homo sapiens GS. A C-beta-Grasp domain and an N-catalytic domain were identified in Tg-GS, indicating that Tg-GS should be classified as a new member of the GS family. A quantitative RT-PCR assay was used to detect mRNA expression of Tg-GS in five different tissues. Higher levels of mRNA expression of GS were detected in the tissues of hemocytes and the mantle. Up-regulation of GS by challenge with the bacteria Vibrio parahaemolyticus and with bacterial wall lipopolysaccharides showed that GS plays a role in anti-bacterial immunity. We conclude that pathogen infection significantly induces expression level of Tg- GS, and that activation of GS influences the immune response of T. granosa by increasing glutamine concentration.

P13 of Leucania separata multiple nuclear polyhedrosis virus affected the polyhedra and budded virions yields of AcMNPV.

p13 gene was first described by our laboratory in Leucania separata multiple nuclear polyhedrovirus (Ls-p13, ORF114) back to 1995. However, the functions of Ls-P13 and its reported homologues remained unknown. In order to probe the function of Ls-P13, recombinant Autographa californica nucleopolyhedroviruses (rAcMNPVs) were constructed to express Ls-P13 in the Sf9 cells at early, late or early/late phase. Observations of microscope showed that the expression of Ls-P13 could decrease the yield of AcMNPV polyhedra in Sf9 cells, and early expressed Ls-P13 had stronger inhibition efficiency than that of the late expressed. Results of flow cytometry also indicated that Ls-P13 decreased the yield of AcMNPV polyhedra while increased those of budded virions (BVs) in Sf9 cells, but the efficacy was lost when its leucine zipper-like domain was mutated. Ls-P13 is a transmembrane protein, which was early located in the nucleus and late mainly in the cytoplasm membrane at 48 h. When its transmembrane domains were deleted, Ls-P13 distribution was dramatically diverted from cytoplasm membrane to nucleus, its corresponding efficacy on polyhedra yield was further increased while that on BVs was slightly weakened. Bioassay results indicated that Ls-P13 accelerated the larvae-killing rate. The mechanism might be that Ls-P13 increased BV yield.