[Corrigendum] Emerging roles of non­coding RNAs in the response of rectal cancer to radiotherapy (Review).

Following the publication of the above review article, the authors have realized that they overlooked including the funding information in the Declarations section. Therefore, the following text should also have been included with the review: Funding: The present review was supported by the National Research Foundation of Korea grant funded by the Korean government (grant no. 2020R1F1A1061122) and Gachon University Research fund of 2018 (GCU-2018-0670) to SH. The authors regret their oversight, apologize to the funding bodies concerned, and regret any inconvenience caused. [the original article was published in International Journal of Oncology 58: 344­358, 2021; DOI: 10.3892/ijo.2021.5175].

Anaplastic lymphoma kinase inhibitor NVP­TAE684 suppresses the proliferation of human pancreatic adenocarcinoma cells.

Anaplastic lymphoma kinase (ALK) is known to be an important therapeutic target in various types of cancer. NVP­TAE684, a well­known inhibitor of ALK, was revealed to exert antitumor effects in several different malignancies. However, the molecular mechanisms responsible for these antitumor effects in cancer cells, including pancreatic adenocarcinoma cells, remain unknown. In the present study, NVP­TAE684 was investigated for its antitumor effects towards pancreatic adenocarcinoma cells. MTT assay, western blot analysis, flow cytometry, caspase­3/7 activity assay and Trypan blue exclusion assay were used and it was revealed that NVP­TAE684 suppressed the proliferation of seven human pancreatic adenocarcinoma cell lines (AsPC­1, Panc­1, MIA PaCa­2, Capan­1, CFPAC­1, Colo­357 and BxPC­3), and significantly increased G2/M arrest and apoptotic cell death. Furthermore, NVP­TAE684 inhibited the phosphorylation of ALK at Y1604, as well as that of downstream mediators such as AKT (S473) and ERK1/2 (Y202/T204). Notably, knocking down ALK with siRNAs also decreased proliferation and promoted G2/M arrest and apoptosis. Furthermore, inhibition of ALK with NVP­TAE684 or siRNA synergistically enhanced gemcitabine­induced cell death by inducing apoptosis. In conclusion, the findings of the present study indicated that NVP­TAE684 exerted its antitumor effects by inducing G2/M arrest and apoptosis via the inhibition of the ALK signaling pathway, and suggests its potential use as an antitumor agent against pancreatic adenocarcinoma.

Inflammasome as a Therapeutic Target for Cancer Prevention and Treatment.

Chronic inflammation is a critical modulator of carcinogenesis through secretion of inflammatory cytokines, which leads to the formation of an inflammatory microenvironment. In this process, the inflammasome plays an important role in the expression and activation of interleukin (IL)-1ß and IL-18 to promote cancer development. The inflammasome is a multiprotein complex consisting of several nucleotide-binding domain and leucine-rich repeat containing receptor, adaptor proteins, and caspase 1 (CASP1). It senses the various intracellular (damage-associated molecular patterns) and extracellular (pathogen-associated molecular patterns) stimuli. A primed inflammasome recruits adaptor proteins, activates CASP1 to enhance the proteolytic cleavage of pro-IL-1ß and IL-18, and sends the signal to respond to each insult. Depending on stimuli and cell contexts, several inflammasomes are closely associated with the initiation and promotion of carcinogenesis. In contrast, inflammasomes also show an ambivalent effect on carcinogenesis by enhancing inflammatory cell death (pyroptosis) and repairing damaged tissues. Although the inflammasome plays a controversial role in carcinogenesis, it may be a promising target for human cancer prevention and treatment. A more in-depth study on the role of the inflammasome in carcinogenesis, based on stimuli, cell contexts, and cancer stages, can lead to the development of novel therapeutic strategies against malignant human cancers.