[Corrigendum] miR­146b­5p inhibits tumorigenesis and metastasis of gallbladder cancer by targeting Toll­like receptor 4 via the nuclear factor­κB pathway.

Following the publication of the article, the authors drew to the Editor's attention that, in Fig. 4D on p. 7, the data correctly shown to represent the E­cadherin bands for the "NOZ" experiment had inadvertently been used to show the Vimentin bands. However, the authors retained their original data, and the corrected version of Fig. 4, now showing the correct data for the Vimentin bands in Fig. 4D for the "NOZ" experiment, is shown on the next page. Note that this error did not grossly affect either the results or the conclusions reported in this work. All the authors agree with the publication of this Corrigendum, and are grateful to the Editor of Oncology Reports for granting them the opportunity to correct the error that was made during the assembly of this figure. Lastly, the authors apologize to the readership for any inconvenience this error may have caused. [Oncology Reports  45: 15, 2021; DOI: 10.3892/or.2021.7966].

miR­146b­5p inhibits tumorigenesis and metastasis of gallbladder cancer by targeting Toll­like receptor 4 via the nuclear factor­κB pathway.

Gallbladder cancer (GBC) is a carcinoma of the biliary tract, which is common in developing countries and is associated with a high fatality rate. The aim of the present study was to investigate the mechanisms underlying the occurrence and development of GBC. A decrease in the expression of miR­146b­5p and an increase in the expression of its target gene Toll­like receptor 4 (TLR4) were first observed in GBC tissues. Further study demonstrated that an increase in TLR4 expression caused by a decrease in miR­146b­5p expression led to activation of nuclear factor (NF)­κB signaling. GBC cells were cultured in vitro, and it was observed that overexpression of miR­146b­5p effectively inhibited their viability, proliferation, migration and invasion, and increased their apoptosis. Using a BALB/c nude mouse xenograft model, it was demonstrated that overexpression of miR­146b­5p was sufficient to reduce tumor volume and alleviate pathological characteristics. Overall, the results of the present study indicated that the decrease in the expression of miR­146b­5p increased TLR4 expression and indirectly activated the NF­κB signaling pathway, thereby regulating the development of GBC.

Curcumin Treatment is Associated with Increased Expression of the N-Methyl-D-Aspartate Receptor (NMDAR) Subunit, NR2A, in a Rat PC12 Cell Line Model of Alzheimer's Disease Treated with the Acetyl Amyloid-ß Peptide, Aß(25-35).

BACKGROUND The aim of this study was to investigate the effect of curcumin treatment on the expression of the N-methyl-D-aspartate receptor (NMDAR) subunit, NR2A, in a rat PC12 cell line treated with the acetyl amyloid-ß peptide, Aß(25-35), in an in vitro model of Alzheimer's disease. MATERIAL AND METHODS PC12 cells, derived from rat phaeochromocytoma, were treated for 24 hours with increasing concentrations of curcumin (5, 10, 20, 30 µM/L) in the presence of the acetyl amyloid-ß peptide, Aß(25-35). A Cell Counting Kit-8 (CCK-8) assay was used to determine cell viability, and flow cytometry was used to measure cell apoptosis. In the supernatant of the treated PC12 cells, Western blotting was used to measure the cell injury biomarker, lactate dehydrogenase (LDH), and the biomarker for oxidative stress, malondialdehyde (MDA). Expression of the N-methyl-D-aspartate receptor (NMDAR) subunit, NR2A, was analyzed by Western blotting and quantitative reverse transcription-polymerase chain reaction (qRT-PCR). RESULTS Curcumin treatment protected the rat PC12 cells from Ab(25-35)-induced reduction in cell viability, apoptosis, release of LDH, and MDA production. Curcumin treatment of PC12 cells was associated with increased expression of the NMDAR subunit, NR2A. CONCLUSIONS The findings of this study showed a neuroprotective effect of curcumin treatment in an in vitro model of Alzheimer's disease that was associated with the increased expression of the NMDAR subunit, NR2A.