[Corrigendum] miR­490­5p regulates the proliferation, migration, invasion and epithelial­mesenchymal transition of pharyngolaryngeal cancer cells by targeting mitogen­activated protein kinase kinase kinase 9.

Following the publication of the above article, an interested reader drew to the authors' attention that the 'Control' and 'NC' data panels for the invasion assay experiments with the FaDu cell line in Fig. 5D on p. 248 contained apparently overlapping data, such that they may have been derived from the same source, even though they were intending to have shown the results from different experiments. On re­examining their original data, the authors have realized that they inadvertently included the data panel correctly shown as the 'NC' experiment for the 'Control' experiment as well. Subsequently, the authors re­examined their figures, and realized that both Figs. 4 and 5 contained additional data panels that had been assembled incorrectly. The authors elected to repeat these experiments in view of the errors made in assembling these figures, and the revised versions of Figs. 4 and 5 are shown on the next two pages. Note that the errors made during the assembly of these figures did not affect the overall conclusions reported in the paper. All the authors agree with the publication of this corrigendum, and are grateful to the Editor of International Journal of Molecular Medicine for allowing them the opportunity to publish this. They also apologize to the readership for any inconvenience caused. [International Journal of Molecular Medicine 44: 240­252, 2019; DOI: 10.3892/ijmm.2019.4196].

miR­490­5p regulates the proliferation, migration, invasion and epithelial­mesenchymal transition of pharyngolaryngeal cancer cells by targeting mitogen­activated protein kinase kinasekinase 9.

MicroRNA (miRNA/miR) has been identified to be a promising tool in treating pharyngolaryngeal cancer. The present study aimed to investigate the role of miR­490­5p in the regulation of proliferation, migration, invasion and epithelial­mesenchymal transition (EMT) of pharyngolaryngeal cancer cells. The data of miR­490­5p expression levels of 45 cases were obtained from the People's Hospital of Xinjiang Uygur Autonomous Region, and the prediction of the target of miR­490­5p was conducted by bioinformatics and verified using a luciferase assay. Cell viability was determined by cell counting kit­8. Migration and invasion rates were measured by wound healing test and Transwell apparatus, respectively. Colony formation rate was measured by plate colony formation assay. mRNA and protein levels were determined by quantitative polymerase chain reaction and western blotting, respectively. miR­490­5p expression was significantly depressed in primary pharyngolaryngeal cancer tissues and cell lines, leading to an unfavorable prognosis. Evidently, miR­490­5p overexpression decreased the cell viabilities of BICR 18 and FaDu cells. Mechanically, miR­490­5p could target mitogen­activated protein kinase kinasekinase 9 (MAP3K9). The overexpression of MAP3K9 could promote cell viability, migration and invasion rates, EMT process and ability of cloning, miR­490­5p could target MAP3K9 and further modulate the proliferation, migration, invasion and EMT of pharyngolaryngeal cancer cells. The results of the present study provide a novel entry point to the treatment of pharyngolaryngeal cancer.