Short rib‑polydactyly syndrome type III (SRPS3) is a lethal perinatal skeletal disorder consisting of polydactyly and multi‑system organ abnormalities. To further assess the pathogenicity of two pairs of compound heterozygotes and to search for novel molecular etiology, X‑rays and hematoxylin and eosin staining were conducted in three cases Two retrospective samples and a newly identified patient with SRPS3. In addition, next‑generation sequencing was used to evaluate a fetus with SRPS3. Typical radiological features of the three cases included a long, narrow thorax with short ribs, shortened long bones, spurs at the metaphysis of the long bones and congenital bowing of the femurs. The present study also observed atypical histopathological changes, together with the absence of proliferation and abundance of retaining cartilage in the primary spongiosum. In addition, two novel compound heterozygous variants were identified in the dynein cytoplasmic 2 heavy chain 1 (DYNC2H1) gene of the fetus NM_001080463.1, c.6591_6593delTGG (chr11103055738‑103055740); NM_001080463.1, c.7883T>C (chr11103070000). The findings of the present study provided further confirmation of the pathogenicity of two compound heterozygous variants in two retrospective samples and identified novel compound heterozygous variants. These findings may improve our knowledge of the histopathological and radiological changes in patients with SRPS3 and the relative effects of DYNC2H1 variants. The findings of the present study may facilitate the clinical and molecular diagnosis of SRPS3.Following the publication of the above paper, a concerned reader drew to the Editor's attention that certain of the western blotting data appeared to have been duplicated, comparing Fig. 2B with Fig. 4A; furthermore, the flow cytometric data panels featured in Fig. U0126 molecular weight 3A appeared to contain repeated patternings of data within those data panels. After having conducted an independent investigation in the Editorial Office, the Editor of Oncology Reports has determined that this paper should be retracted from the Journal on account of a lack of confidence concerning the originality and the authenticity of the data. The authors were asked for an explanation to account for these concerns, but the Editorial Office never received any reply. The Editor regrets any inconvenience that has been caused to the readership of the Journal. [the original article was published in Oncology Reports 35 2364‑2372, 2016; DOI 10.3892/or.2016.4612].Intervertebral disc degeneration (IDD) is a common chronic disease characterized by the loss of extracellular matrix (ECM) in the nucleus pulposus (NP). Accumulating evidence has revealed that abnormal expression of microRNAs (miRs) is closely associated with IDD development. The present study aimed to investigate the precise role and possible mechanism underlying the effects of miR‑654‑5p in the pathogenesis of IDD. NP cells were isolated from patients with IDD. Monodansylcadaverine staining was conducted to reveal cell autophagy, while western blotting was performed to detect the expression of ECM‑related proteins in NP cells. Luciferase reporter and RNA immunoprecipitation assays were conducted to identify the binding between RNAs. The results demonstrated that miR‑654‑5p was significantly upregulated in degenerated NP tissues from patients with IDD and high miR‑654‑5p expression was positively associated with disc degeneration grade. Functional assays suggested that miR‑654‑5p facilitated ECM degradation by increasing the expression levels of MMP‑3, MMP‑9 and MMP‑13, as well as decreasing collagen I, collagen II, SOX9 and aggrecan expression by inhibiting autophagy. Furthermore, autophagy‑related gene 7 (ATG7) was verified as a direct downstream target gene of miR‑654‑5p. miR‑654‑5p could bind to the 3' untranslated region of ATG7 to inhibit its mRNA expression and further reduce its translation. Notably, ATG7 knockdown abrogated the effects of the miR‑654‑5p inhibitor on ECM degradation and autophagy regulation. Furthermore, miR‑654‑5p inhibited autophagy in NP cells by increasing the protein expression levels of phosphorylated (p)‑PI3K, p‑AKT and p‑mTOR in an ATG7‑dependent manner. In conclusion, the results of the present study revealed that miR‑654‑5p may enhance ECM degradation via inhibition of autophagy by targeting ATG7 to activate the PI3K/AKT/mTOR signaling pathway. These findings may provide novel insights into the treatment of IDD.p53‑reactivation and induction of massive apoptosis‑1, APR‑017 methylated (PRIMA‑1met; APR246) targets mutant p53 to restore its wild‑type structure and function. It was previously demonstrated that PRIMA‑1met effectively inhibited the growth of colorectal cancer (CRC) cells in a p53‑independent manner, and distinctly induced apoptosis by upregulating Noxa in p53‑mutant cell lines. The present study including experiments of western blotting, acridine orange staining and transmission electron microscopy revealed that PRIMA‑1met induced autophagy in CRC cells independently of p53 status. Importantly, PRIMA‑1met not only promoted autophagic vesicle (AV) formation and AV‑lysosome fusion, but also increased lysosomal degradation. Furthermore, Cell Counting Kit‑8 assay, colony formation assay and small interfering RNA transfection were performed to investigate the underling mechanisms. The study indicated that activation of the mTOR/AMPK‑ULK1‑Vps34 autophagic signaling cascade was key for PRIMA‑1met‑induced autophagy. Additionally, autophagy served a crucial role in the inhibitory effect of PRIMA‑1met in cells harboring wild‑type p53, which was closely associated with the increased expression of Noxa. Taken together, the results determined the effect of PRIMA‑1met on autophagy, and further revealed mechanistic insights into different CRC cell lines. It was concluded that PRIMA‑1met‑based therapy may be an effective strategy for CRC treatment.Following the publication of the above paper, a concerned reader drew to the Editor's attention that several figures (principally, Figs. 3, 6 and 8) contained data that bore striking similarities to data published in other papers, some of which had been published around the same time and written by different authors based at different research institutions. After having conducted an independent investigation in the Editorial Office, the Editor of Molecular Medicine Reports has determined that this article should be retracted from the Journal on account of a lack of confidence concerning the originality and the authenticity of the data. The authors were asked for an explanation to account for these concerns, but the Editorial Office never received any reply. The Editor regrets any inconvenience that has been caused to the readership of the Journal. [the original article was published in Molecular Medicine Reports 12 5012‑5018, 2015; DOI 10.3892/mmr.2015.4033].