[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.