Silibinin, an effective anti-cancer and chemopreventive agent in various epithelial cancer models, has been reported to inhibit cancer cell growth through mitogenic signaling pathways. However, whether it can inhibit human pancreatic carcinoma growth and what are the underlying mechanisms is still not well elucidated. Here, we evaluated the inhibitory proliferation effects of Silibinin in pancreatic carcinoma growth and examined whether Silibinin modulates cell cycle and apoptosis. Our results indicate that Silibinin effectively inhibited the pancreatic carcinoma AsPC-1, BxPC-3 and Panc-1 cells’ proliferation and caused apoptosis. Silibinin induced a decrease in S phase and cell cycle arrest in G1 phase in AsPC-1 cells, but had no obvious changes in BxPC-3 and Panc-1 cell cycle. Furthermore, these results suggest that Silibinin might be a candidate chemopreventive agent for pancreatic carcinoma therapy.

Tea is believed to be beneficial for health, and the effects of the fermentation process on its contributions to apoptosis and cell cycle arrest of gastric cancer cells have not been completely investigated. In this study, the chemical components in green tea, black tea and pu-erh tea aqueous extracts were analyzed and compared. The polysaccharide and caffeine levels were substantially higher in the fermented black tea and pu-erh tea, while the polyphenol level was higher in the unfermented green tea. Hence, a treatment of tea aqueous extract and the components, which are emerging as promising anticancer agents, were pursued to determine whether this treatment could lead to enhance apoptosis and cell cycle arrest. In the human gastric cancer cell line SGC-7901, the cell viability and flow cytometry analysis for apoptotic cells indicated effects in a dose-dependent inhibition manner for the three tea treatment groups. The apoptosis rates were found to be elevated after 48 h of treatment with 31.2, 125, and 500 μg/mL of green tea extract, the higher catechins content may be involved in the mechanism. Cell cycle was arrested in S phase in the fermented black tea and pu-erh tea, and the populations were significantly decreased in G2/M phases, possibly due to the oxidation of tea polyphenols, which causes an increase of theabrownins. CCC-HEL-1 normal cells were not sensitive to tea extract. These findings suggest that the fermentation process causes changes of the compounds which might be involved in the changes of cell proliferation inhibition, apoptosis induction and cell cycle arrest.

The tumor suppressor p53 serves important roles in cell cycle arrest and apoptosis, and its activation increases the sensitivity of cancer cells to radiotherapy or chemotherapy. In the present study, the small molecule 2-[1-(4-(benzyloxy)phenyl)-3-oxoisoindolin-2-yl)-2-(4-methoxyphenyl)] acetic acid (CDS-3078) significantly increased p53 mRNA expression levels in a dose-dependent manner. Treatment with CDS-3078 increased p53 expression levels and p53-mediated activation of its downstream target genes in HeLa cells. Additionally, p53^+/+ HeLa cells treated with CDS-3078 presented with dysfunctional mitochondria, as indicated by the decrease in Bcl-2 levels, the increase in Bcl-2 homologous antagonist killer and the increase in cytochrome c release from the mitochondria to the cytoplasm. The present results suggested that CDS-3078 treatment significantly induced G₂/M phase cell cycle arrest. Therefore, CDS-3078 administration induced apoptosis via p53-mediated cell cycle arrest, causing mitochondrial dysfunction and resulting in apoptotic cell death in cervical cancer cells. Collectively, the present results suggested that CDS-3078 may be a potential anticancer agent.

Subsequently to the publication of the above article, an interested reader drew to the Editor’s attention that there may have been an issue of non‑specificity associated with the choice of the anti‑Bax antibody (sc‑7480) in light of a publication that appeared in the journal Cell Death & Disease written by Entrop and colleagues on this issue; furthermore, it was noted that, for the western blots shown in Fig. 3A on p. 6, there appeared to have been a duplication of data that concerned the Procaspase 3/Cleavage caspase 3 and Procaspase 9/Cleavage caspase 9 experiments. First, the authors acknowledged the possibility of false‑positive results using the anti‑Bax antibody, although they did not identify any regulatory effects of the small‑molecule CDS‑3078 using this antibody in their experiments; furthermore, the regulatory effects of CDS‑3078 were explored on the basis of its influence on the proteins Bcl‑2, Bak and cytochrome c, which was sufficient to demonstrate its ability to induce apoptosis. Secondly, they realized that Fig. 3 had inadvertently been assembled incorrectly; however, the authors had retained their orginal data, and were able to provide a revised version of Fig. 3, now featuring the correct data for the Procaspase 9/Cleavage caspase 9 experiment. The revised version of Fig. 3 is shown on the next page. Note that the error made in the assembly of Fig. 3 did not have a major impact on either the overall results or on the conclusions reported in this study. All the authors agree with the publication of this corrigendum, and are grateful to the Editor of Experimental and Therapeutic Medicine for granting them the opportunity to publish this; furthermore, they apologize to the readership for any inconvenience caused. [Experimental and Therapeutic Medicine 20: 284, 2020; DOI: 10.3892/etm.2020.9414]