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This document is a retraction notice for an article titled "SIRT6 Overexpression Induces Apoptosis of Nasopharyngeal Carcinoma by Inhibiting NF-κB Signaling." The retraction is due to concerns about the duplication of images from other unrelated articles. The authors were unable to provide an explanation for the duplicated images or data for the study. The article will remain online but will be marked as "Retracted." [Extracted from the article]

Purpose: Our previous study has revealed that T-lymphoma invasion and metastasis-inducing factor 1 (Tiam1) overexpression are significantly associated with aggressive behavior and poor prognosis in patients with laryngeal squamous cell carcinoma (LSCC). However, the influence of Tiam1 in the radioresistance of LSCC and its mechanism have never been elucidated. Materials and Methods: Western blotting was used to confirm the relationship between Tiam1 and the JNK/ATF-2 signaling pathway. To explore the specific functions of Tiam1 and JNK/ATF-2 signaling pathway on the proliferation and apoptosis of LSCC after radiation, cloning formation assay and flow cytometry were conducted in vitro, and the experiments on a xenograft mouse model and TUNEL assay were performed in vivo. Results: Western blotting indicated that Tiam1 can regulate the JNK/ATF-2 signaling pathway through the influence of the activity of JNK and ATF-2. Up-regulation of Tiam1 could promote proliferation and inhibit apoptosis of LSCC after radiation both in vitro and in vivo. Moreover, the down-regulation of the JNK/ATF-2 signaling pathway reduced the radioresistance of LSCC caused by Tiam1 up-regulation. Conclusion: These results suggest that the up-regulation of Tiam1 expression can promote the radioresistance of LSCC through activation of the JNK/ATF-2 signaling pathway. [ABSTRACT FROM AUTHOR]

Background: Previous reports show that SIRT6 serves as a critical modulator of the development of multiple malignancies as well as other disorders. However, its role in nasopharyngeal carcinoma (NPC) is unknown. Thus, we elucidated the effects of SIRT6 on the survival of NPC cells, and modulation of cell death.Methods: We found that expression of SIRT6 is downregulated in ten human NPC specimens as well as in the human NPC cell lines, 5-8 F and CNE1, as compared with that in healthy tissues and normal nasopharyngeal NP69 cells. The MTT assay and colony formation assay revealed that upregulation of SIRT6 impaired the proliferation, as well as the survival of 5-8 F and CNE1 cells. The TUNEL assay, annexin V-FITC/propidium iodide, and flow cytometry were performed to detect apoptosis. The results revealed that the expression of SIRT6 resulted in increased apoptosis.Results: Western blotting results showed that SIRT6 overexpression decreased anti-apoptotic Bcl-2 levels, whereas it promoted an increase in pro-apoptotic Bax and cleaved caspase-3 levels. Moreover, NF-κB levels were markedly reduced in cells expressing SIRT6, whereas they were increased in cells transfected with shRNA-SIRT6. Recovery of NF-κB expression was found to counter the suppressive influence of SIRT6 on NPC cell survival, whereas, NF-κB knockdown increased apoptosis of NPC cells.Conclusion: Thus, the findings of our study offer insight into the biological and molecular mechanisms underlying the development of NPC and may lead to the development of new and innovative strategies for the treatment of NPC. [ABSTRACT FROM AUTHOR]