[Corrigendum] Hsa­circRNA­G004213 promotes cisplatin sensitivity by regulating miR­513b­5p/PRPF39 in liver cancer.

Following the publication of the above article, the authors have realized that, on p. 8, some of the supplementary data were cited incorrectly in the main text. In the right-hand column, second paragraph, the sentence beginning on line 5 should have read as follows (changed text is highlighted in bold): "Meanwhile, the expression of miR­513b­5p in tumor tissues was decreased and the expression of PRPF39 was increased in tumor tissues with knockout of circ­G004213 (Fig. S3D and E)." (i.e., the reference to Fig. S3C and D was incorrect.). The authors regret their oversight in failing to correct the inaccurate citation of the data in the paper, are grateful to the Editor for allowing them the opportunity to publish this Corrigendum, and apologize to the readership for any inconvenience caused. [the original article was published in Molecular Medicine Reports 23: Article no. 421, 2021; DOI: 10.3892/mmr.2018.12060].

[Corrigendum] High glucose promotes tumor cell proliferation and migration in lung adenocarcinoma via the RAGE­NOXs pathway.

Following the publication of the above article, the authors have realized that the Materials and methods section and Figs. 1, 3 and 4 contained certain errors. In the Materials and methods section, the high glucose concentration was reported incorrectly as being 25 mmol/l; this should have been stated as 15 mmol/l. Furthermore, the normal concentration of glucose should have been reported as 5 mmol/l rather than  5.5 mmol, and the glucose concentration gradient should have been written as 0, 5, 10, and 15 mmol/l, and not as 0, 5, 10, and 25 mmol/l. Secondly, the authors have corrected some miscalculations associated with the bar charts featured in Figs. 1, 3, and 4, and the revised versions of these figures are shown here. All these corrections were approved by all authors. The authors regret that these errors were included in the paper, even though they did not substantially alter any of the major conclusions reported in the study, and apologize to the readership for any inconvenience caused. [the original article was published in Molecular Medicine Reports 17: 8536­8541, 2018; DOI: 10.3892/mmr.2018.8914].

High glucose promotes tumor cell proliferation and migration in lung adenocarcinoma via the RAGE­NOXs pathway.

Over the past few decades, it has been demonstrated that hyperglycemia can promote lung carcinoma growth, potentially through significantly increased glucose metabolism; however, the underlying mechanism remains to be fully elucidated. In the present study, treatment with a high concentration of glucose (HG) significantly promoted the proliferation and migration of A549 cells. Receptor for advanced glycation end­products (RAGE) has previously been demonstrated to be associated with diabetes mellitus and oxidative stress, and nicotinamide adenine dinucleotide phosphate oxidases (NOXs) are considered to be initiating factors of oxidative stress. Therefore, an MTT assay, wound­healing assay, quantitative polymerase chain reaction and western blotting assays were used to analyze the RAGE­NOX­4 pathway and to determine its potential involvement in glycometabolism­associated tumorigenesis. The present study demonstrated that HG could increase the protein expression of RAGE and NOX­4, whereas the inhibitor of RAGE (anti­RAGE antibody) could suppress this effect. Futhermore, the inhibitor of NOX [diphenyl iodonium chloride (DPI)] could reduce the protein expression of RAGE and NOX­4. Furthermore, inhibition of RAGE led to the downregulation of vascular endothelial growth factor (VEGF) and hypoxia­inducible factor­1α (HIF­1α), thus suggesting that HG may influence angiogenesis and tumor metabolism via the RAGE­NOXs pathway. The present study also demonstrated that the RAGE­blocking antibody downregulated NOX­4 and subsequently reduced the production of downstream inflammatory factors, whereas DPI did not affect the mRNA expression of RAGE but it did reduce the protein level of RAGE and then attenuate the inflammatory response. These results indicated that inhibition of RAGE or NOXs may promote the reduced expression of VEGF and HIF­1α, and NOXs may be downstream targets of RAGE, thus indicating a HG­RAGE­NOXs­VEGF/HIF­1α association. Furthermore, the results indicated that HG may serve a role in the development of lung adenocarcinoma, mediated by the RAGE­oxidative stress pathway; therefore, the regulation of this glucose­associated pathway may be a promising novel direction for oncotherapy. However, while certain antidiabetic agents have been verified to exert inhibitory effects on tumor growth, they can also have long­term adverse effects on the body, which may limit the value of these drugs as anticancer treatments. In conclusion, the present study suggested a novel attempt to suppress glucose­induced tumor growth using a RAGE inhibitor such as soluble RAGE while avoiding the risk of glucose fluctuation.