[Retracted] Downregulation of CKS1B restrains the proliferation, migration, invasion and angiogenesis of retinoblastoma cells through the MEK/ERK signaling pathway.

Following the publication of the above paper, it has been drawn to the Editors' attention by a concerned reader that certain of the lumen formation assay data shown in Fig. 5A on p. 112 were strikingly similar to data appearing in different form in another article written by different authors at different research institute, which had already been published in the journal Biomedicine & Pharmacotherapy prior to the submission of this paper to International Journal of Molecular Medicine, and which has also subsequently been retracted. In view of the fact that the contentious data had already apparently been published previously, the Editor of International Journal of Molecular Medicine has decided that this paper should be retracted from the Journal. After having been in contact with the authors, they agreed with the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Molecular Medicine 44: 103­114, 2019; DOI: 10.3892/ijmm.2019.4183].

Downregulation of CKS1B restrains the proliferation, migration, invasion and angiogenesis of retinoblastoma cells through the MEK/ERK signaling pathway.

Retinoblastoma (RB) is a common neoplasm that is exhibited in individuals globally. Increasing evidence demonstrated that cyclin­dependent kinase regulatory subunit 1B (CKS1B) may be involved in the pathogenesis of various tumor types, including multiple myeloma and breast cancer. In the present study, the hypothesis that CKS1B downregulation would effectively inhibit the proliferation, invasion and angiogenesis of RB cells through the mitogen­activated protein kinase kinase (MEK)/extracellular signal­regulated kinase (ERK) signaling pathway was examined. Initial investigation of the expression profile of CKS1B in RB and adjacent retina tissues was performed using reverse transcription­quantitative polymerase chain reaction and western blot analysis. A total of three RB cell lines, SO­RB50, Y79 and HXO­RB44, were examined for selection of the cell line with the highest expression of CKS1B, and human normal retinal vascular endothelial cells (ACBRI­181) were also evaluated. CKS1B short hairpin RNA (shRNA) sequences (shRNA CKS1B­1, shRNA CKS1B­2 and shRNA CKS1B­3) and negative control shRNA sequences were constructed and transfected into cells at the third generation to evaluate the role of shCKS1B and the MEK/ERK signaling pathway in RB. Furthermore, the effect of shCKS1B on cell proliferation, migration, invasion, apoptosis and angiogenesis was investigated. CKS1B was determined to be highly expressed in RB tissue, compared with adjacent retina tissue. SO­RB50 and HXO­RB44 cells treated with shRNA CKS1B­1 and shRNA CKS1B­2 were selected for the present experiments. Activation of the MEK/ERK signaling pathway increases the expression of MEK, ERK, B­cell lymphoma 2, proliferating cell nuclear antigen, cyclin D1, vascular endothelia growth factor and basic fibroblast growth factor, enhances cell proliferation, migration, invasion and lumen formation, and decreases apoptosis. Following silencing CKS1B, the aforementioned conditions were reversed. The key observations of the present study demonstrated that shCKS1B can inhibit the proliferation, invasion and angiogenesis of RB cells by suppressing the MEK/ERK signaling pathway. Thus, CKS1B represents a potential research target in the development of therapeutics for RB.

Kangxian capsules: Effects on convulsive injuries, N-methyl-d-aspartate (NMDA) receptor subunit expression, and free Ca(2+) concentration in a rat hippocampal neuron epileptic discharge model.

PURPOSE: To investigate the effects and mechanisms of Kangxian (KX) capsules on hippocampal neuron convulsive injuries. METHODS: An epileptic discharge model was prepared with hippocampal neurons and divided into groups that were subjected to control, Mg-free, MK801, or anti-epilepsy (KX) interventions for 6 or 24h. The N-methyl-d-aspartate (NMDA) receptor channel current was recorded with a whole-cell patch-clamp technique, and the decay tau was determined from the receptor channel attenuation. The NMDA receptor subunits (NR1, NR2A, and NR2B) were detected by immunoblot assays, and intracellular free Ca(2+) was detected by laser confocal microscopy. RESULTS: The discharge times (6h: 100.66±36.51min, 24h: 134.42±86.43min) and tau values (6h: 934.0±564.9s, 24h: 846.6±488.0) of the Mg-free group were significantly increased (P<0.05) compared to the control group. All of the groups had similar levels of NR1 expression. NR2A and NR2B expression was significantly decreased in the Mg-free group and significantly increased most in the MK801 group, which was followed by the KX group (P<0.01). The free Ca(2+) concentrations in the control group were lower than those in the MK-801 and KX groups, the concentrations of which were significantly lower than those in the Mg-free group and which decreased with time. CONCLUSION: Kangxian capsules played its antiepileptic and neuroprotective roles via multiple targets and the underlying mechanisms included acceleration of the attenuation time course of NMDA receptor channels, alterations in the expression of NMDA receptor subunits, and reductions in the concentration of intraneuronal Ca(2+).