Retraction Note: MiR-221 inhibits proliferation of pancreatic cancer cells via down regulation of SOCS3.

The article "MiR-221 inhibits proliferation of pancreatic cancer cells via down regulation of SOCS3", by J. Xie, J.-T. Wen, X.-J. Xue, K.-P. Zhang, X.-Z. Wang, H.-H. Cheng, published in Eur Rev Med Pharmacol Sci 2018; 22 (7): 1914-1921-DOI: 10.26355/eurrev_201804_14714-PMID: 29687843 has been retracted by the Editor in Chief for misconduct and data fabrication. An investigation conducted by the National Health Commission of the People's Republic of China, determined that the information and images presented in the paper have been manipulated, pieced together, and subjected to various fraudulent alterations. Consequently, the Editor in Chief mistrusts the results presented and has decided to withdraw the articles. The corresponding authors did not respond to journal correspondence about the investigation and retraction of this article. This article has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/14714.

MiR-221 inhibits proliferation of pancreatic cancer cells via down regulation of SOCS3.

OBJECTIVE: The over-activation of Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathway induced by cytokines are closely correlated with tumorigenesis. Suppressor of cytokine signaling 3 (SOCS3) serves as a negative regulator for JAK-STAT, and its down-regulation is involved in the oncogenesis of pancreatic cancer. We aimed at investigating the effect of miR-221 on the expression and proliferation, cycle and apoptosis of pancreatic cancer cells and determine the related mechanism. PATIENTS AND METHODS: Dual luciferase reporter gene assay was used to analyze the regulation between miR-221 and SOCS3. The expressions of miR-221, SOCS3, p-JAK and p-STAT3 in normal human pancreatic epithelial cell HPDE6-C7 and pancreatic cancer cell PANC-1 were quantified by qPCR and Western blot. Flow cytometry was used to identify cell cycle and proliferation. In vitro cultured PANC-1 cells were transfected with miR-221 inhibitor or pIRES2-SOCS3. The expressions of miR-221, SOCS3, p-JAK and p-STAT3, along with the cell proliferation or apoptosis, were compared. RESULTS: Bioinformatics analysis showed the existence of binding site between miR-221 and 3'-UTR of SOCS3 mRNA. Dual luciferase gene reporter assay confirmed the targeted regulation between miR-221 and SOCS3. Compared to HPDE6-C7 cells, higher levels of miR-221, p-JAK and p-STAT3 expression, and lower expression of SOCS3, were found in PANC-1 cells, along with the increase of cell proliferation. Transfection of miR-221 inhibitor or pIRES2-SOCS3 remarkably enhanced SOCS3 expression, inhibited the levels of p-JAK and p-STAT3 expression, and impeded the proliferation of PANC-1 cells. CONCLUSIONS: MiR-221 decreases proliferation potency of PANC-1 cells and affects JAK-STAT3 signaling pathway via inhibiting SOCS3.

Role of Th1/Th2 cytokines in the diagnosis and prognostic evaluation of ankylosing spondylitis.

Ankylosing spondylitis (AS), a progressive disease of the spine, manifests as peripheral arthritis with tendon and ligament inflammation that restricts activity. AS is a rheumatoid autoimmune disease although the rheumatoid factor is absent in patients with AS. It is characterized by inflammatory changes such as elevated levels of serum inflammatory factors. The roles of Th1 and Th2 cytokines in autoimmune diseases are well known. However, the roles of these cytokines in the diagnosis and prognosis of AS is poorly understood. The aim of this study was to investigate the roles of Th1/Th2 cytokines in the diagnosis and prognosis of AS. The BASDAI activity, BASFI functional index, BASMI measurement score, and the levels of CRP and ESR were measured during the treatment of patients with active AS. The levels of IFN-γ and TNF-α (Th1 cytokines) and IL-4 and IL-10 (Th2 cytokines) were quantified. The levels of IL-4 and IL-10 were significantly low in the serum of patients with active AS, who also had high IFN-γ and TNF-α levels compared to those in the control individuals (P < 0.05). After treatment, the levels of IL-4 and IL-10 increased while those of IFN-γ and TNF-α decreased compared to those in individuals with active AS (P < 0.05). The disease activity index correlated positively with levels of IFN-γ and TNF-α and negatively with levels of IL-4 and IL-10, but not with that of CRP or ESR. Changes in the levels of Th1/2 cytokines in patients with AS may reflect disease activity and prognosis.

Multidrug-resistant genes of aminoglycoside-modifying enzymes and 16S rRNA methylases in Acinetobacter baumannii strains.

We examined the distribution of genes of aminoglycoside-modifying enzymes and 16S rRNA methylases in multidrug-resistant Acinetobacter baumannii to explore the association of these genes with drug resistance. Strains isolated from clinical specimens were screened using an automatic microbial identification system, and 9 aminoglycoside-modifying enzyme and 6 16S rRNA methylase genes were analyzed using polymerase chain reaction and verified by DNA sequencing. Next, sequence alignment was carried out using the Chromas software and a susceptibility test was performed using the Kirby-Bauer disk diffusion method. Genes encoding aminoglycoside-modifying enzymes were detected in all 20 strains of multidrug-resistant A. baumannii. The positive rates of aac(3')-I, aac(6')-Ib, ant(3'')-I, and aph(3')-I were 90.0, 90.0, 85.0, and 35.0%, respectively. However, genes encoding 16S rRNA methylases were not positively detected in the 20 strains of multidrug-resistant A. baumannii. The resistance of multidrug-resistant A. baumannii may be associated with aminoglycoside-modifying enzyme genes but not with 16S rRNA methylase genes.

Regulation of Caco-2 cell proliferation by basolateral membrane epidermal growth factor receptors.

The epidermal growth factor (EGF) receptor is an important mediator of intestinal epithelial cell proliferation. We studied cell-surface localization of this molecule in Caco-2 cells and characterized cellular responses to apical or basolateral EGF stimulation. 125I-labeled EGF bound almost exclusively to a 180-kDa molecule, existing as a single high-affinity population by Scatchard analysis. On basolateral membranes 13- to 15-fold more ligand binding was seen. Apical/basolateral differences were not significantly altered by incubation with either blocking antibody to EGF receptor or transforming growth factor-alpha (TGF-alpha) neutralizing antibody. Even though apical EGF receptors were demonstrated, only basolateral membrane stimulation with EGF increased tyrosine kinase activity and enhanced uptake of [3H]thymidine. Continuous exposure to EGF during culture significantly increased monolayer DNA content. These data demonstrate that Caco-2 cell proliferation is driven solely by basolateral membrane EGF receptor, despite the presence of lesser amounts of this molecule on the apical surface. Differences between apical and basolateral membrane receptor expression are not the result of polarized secretion of TGF-alpha or other EGF receptor ligands.