[Corrigendum] PRIMA­1met induces autophagy in colorectal cancer cells through upregulation of the mTOR/AMPK­ULK1­Vps34 signaling cascade.

Following the publication of the above article, the authors contacted the Editorial Office to explain that the strips of ß­actin, LC3 and p62 proteins of the RKO cell line shown in Fig. 2A and B, and those of the SW620 cell line shown in Fig. 3A and B, were assembled in these figures incorrectly. To rectify the presentation of these two figures, the authors proposed that they replace the strips of ß­actin and p62 proteins in the original Figs. 2B and 3B with the ß­actin bands from one of the repeated western blotting experiments.  The revised and corrected versions of Figs. 2 and 3 are shown on the next page. The authors wish to emphasize that these corrections do not grossly affect either the results or the conclusions reported in this work. The authors all agree to the publication of this Corrigendum, and are grateful to the Editor of Oncology Reports for granting them the opportunity to correct the errors that were made during the assembly of these figures. Lastly, the authors apologize to the readership for any inconvenience these errors may have caused. [Oncology Reports 45: 86, 2021; DOI: 10.3892/or.2021.8037].

PRIMA­1met induces autophagy in colorectal cancer cells through upregulation of the mTOR/AMPK­ULK1­Vps34 signaling cascade.

p53­reactivation and induction of massive apoptosis­1, APR­017 methylated (PRIMA­1met; APR246) targets mutant p53 to restore its wild­type structure and function. It was previously demonstrated that PRIMA­1met effectively inhibited the growth of colorectal cancer (CRC) cells in a p53­independent manner, and distinctly induced apoptosis by upregulating Noxa in p53­mutant cell lines. The present study including experiments of western blotting, acridine orange staining and transmission electron microscopy revealed that PRIMA­1met induced autophagy in CRC cells independently of p53 status. Importantly, PRIMA­1met not only promoted autophagic vesicle (AV) formation and AV­lysosome fusion, but also increased lysosomal degradation. Furthermore, Cell Counting Kit­8 assay, colony formation assay and small interfering RNA transfection were performed to investigate the underling mechanisms. The study indicated that activation of the mTOR/AMPK­ULK1­Vps34 autophagic signaling cascade was key for PRIMA­1met­induced autophagy. Additionally, autophagy served a crucial role in the inhibitory effect of PRIMA­1met in cells harboring wild­type p53, which was closely associated with the increased expression of Noxa. Taken together, the results determined the effect of PRIMA­1met on autophagy, and further revealed mechanistic insights into different CRC cell lines. It was concluded that PRIMA­1met­based therapy may be an effective strategy for CRC treatment.

Analysis of the association of single nucleotide polymorphisms of interleukin-23 receptor (IL-23R) and inflammatory bowel disease in a Chinese Han cohort.

Inflammatory bowel disease (IBD) is a chronic, complex genetic disease with rapidly increasing prevalence in China. The interactions of genetic, environmental, and microbial factors contribute to the development of IBD, however, the precise etiologies of IBD are not well understood yet. Interleukin-23 receptor (IL-23R) encodes a subunit of receptor for IL-23, which is an important proinflammatory cytokine. In this study, we investigated the relationship between the single nucleotide polymorphism (SNP) of IL-23R gene and IBD in Chinese Han population. We genotyped three nonsynonymous IL-23R SNPs with amino acid changes (rs11209026, p.Arg381Gln; rs41313262 p.Val362Ile and rs11465797 p.Thr175Asn) in 198 patients with IBD (124 UC and 74 CD) and 100 healthy controls. The prevalence of the A allele in IL-23R Arg381Gln of CD appeared less than controls, but it was not statistically significant (2.70% vs. 6.00%, p > 0.05). There was no statistical difference between UC and controls (5.65% vs. 6.00%, p = 0.91). The p.Val362Ile variant was present in 2.42% of UC patients, in 2.70% of CD patients, which was similar in the control (2.00%). There was no statistical difference among these three groups. We did not detect Thr175Asn (rs11465797 c.524 C>A) in all the three groups. In conclusion, our study demonstrated that the p.Val362Ile and Arg381Gln were not associated with susceptibility to IBD in Chinese Han population.