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The results revealed an increased apoptosis rate, and reduced cell proliferation and oxidative stress in H2‑treated HeLa cells but not in HaCaT cells. Similarly, decreased tumor growth and cell proliferation, and enhanced cell apoptosis were observed in H2‑treated HeLa tumors. RNA sequencing and GO analysis suggest that downregulated HIF1A (HIF‑1α mRNA) and RelA (NF‑κB p65) levels, and reduced NF‑κB signaling were associated with the antitumor effect of H2. https://www.selleckchem.com/products/cftrinh-172.html Finally, decreased HIF‑1α and NF‑κB p65 expression both at the transcriptional and translational levels were observed in H2‑treated HeLa cells and in HeLa‑derived tumors. In conclusion, the present study reveals a novel mechanism of H2 against cervical cancer, which may serve as a potential therapeutic target in clinical practice.Tumor necrosis factor‑related apoptosis‑inducing ligand (TRAIL) is a cytokine with the potential to induce cancer cell‑specific apoptosis with minimal toxicity to normal cells. Therefore, the resistance of certain cancer cells to TRAIL is a major concern and agents that can either enhance TRAIL capabilities or overcome TRAIL resistance are necessary for the development of cancer treatments. The present study investigated whether the antidepressant drug amitriptyline could sensitize TRAIL‑resistant A549 lung cancer cells and enhance TRAIL‑induced apoptosis. Antidepressants are usually prescribed to cancer patients to relieve emotional distress, such as depression or dysthymia. The present study revealed for the first time, to the best of our knowledge, that amitriptyline increased death receptor (DR) 4 and 5 expression, a requirement for TRAIL‑induced cell death. Genetic inhibitors of DR4 and DR5 significantly reduced amitriptyline‑enhanced TRAIL‑mediated apoptosis. Additionally, the present study explored whether blocking autophagy increased DR4 and DR5 expression. Blocking autophagy flux with the final stage autophagy inhibitor chloroquine (CQ) also upregulated DR4 and DR5 expression. TRAIL in combination with amitriptyline or CQ significantly increased the expression of apoptosis‑indicator proteins cleaved caspase‑8 and caspase‑3. The expression levels of LC3‑II and p62 were significantly higher in amitriptyline‑treated cells, which confirmed that amitriptyline blocks autophagy by inhibiting the fusion of autophagosomes with lysosomes. Overall, the present results contributed to understanding the mechanism responsible for the synergistic anticancer effect of amitriptyline and TRAIL and also presented a novel mechanism involved in DR4 and DR5 upregulation.Aberrant expression of circular RNAs (circRNAs) has been demonstrated to be related to the development of colorectal cancer (CRC), the third most common cancer worldwide. However, the mechanism of the effect of circRNA NOP2/Sun domain family, member 2 (circNSUN2) on the malignant biological behavior of CRC remains unclear. In the present study, the expression of circNSUN2 and microRNA (miR)‑181a‑5p was detected by RT‑qPCR. The expression of Rho‑associated coiled‑coil‑containing protein kinase 2 (ROCK2) was measured by western blotting. Cell proliferation was detected by CCK‑8 assay. The cell apoptosis rate was measured by flow cytometry. Cell migration ability was evaluated by Transwell assay. The interactions between circNSUN2, miR‑181a‑5p and ROCK2 were verified by dual‑luciferase reporter assay. The results revealed that circNSUN2 was highly expressed in CRC tissues and cell lines. Knockdown of circNSUN2 inhibited the malignant biological behavior of CRC in vivo and in vitro. Moreover, miR‑181a‑5p was revealed to be a target gene of circNSUN2, and the expression of ROCK2 was negatively regulated by miR‑181a‑5p. Knockdown of circNSUN2 inhibited proliferation and migration, and induced apoptosis of CRC cells and suppressed tumor growth by targeting miR‑181a‑5p to decrease ROCK2 expression. In conclusion, circNSUN2 promoted the progression of CRC by sponging miR‑181a‑5p to increase the expression of ROCK2.Nasopharyngeal carcinoma (NPC) is a common malignant tumor in South China and is characterized by a high death rate. Ophiopogonin B (OP‑B) is a bioactive component of Radix Ophiopogon japonicus, which is frequently used in traditional Chinese medicine to treat cancer. The present study aimed to examine the anti‑cancer properties of OP‑B on NPC cells. Cell viability and cell proliferation were measured using MTT and EdU assays. Flow cytometry was used to measure cell apoptosis, reactive oxygen species and mitochondrial membrane potential. Western blotting was used to investigate the expression of apoptosis and Hippo signaling pathway proteins. OP‑B inhibited the proliferation of NPC cells by inducing apoptosis and disturbing the mitochondrial integrity. OP‑B enhanced ROS accumulation. In addition, OP‑B promoted the expression of mammalian STE20‑like kinase 1, large tumor suppressor 1 and phosphorylated yes‑associated protein (YAP) and suppressed the expression of YAP and transcriptional enhanced associate domain in NPC cells. OP‑B increased the expression of forkhead box transcription factor O1 in the nuclear fraction. In conclusion, OP‑B has therapeutic potential and feasibility in the development of novel YAP inhibitors for NPC.Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that certain of the western blotting data shown in Figs. 4C, 5B and 6D were strikingly similar to data appearing in different form in other articles by different authors. Owing to the fact that the contentious data in the above article were already under consideration for publication, or had already been published, elsewhere prior to its submission to Oncology Reports, the Editor has decided that this paper should be retracted from the Journal. After having been in contact with the authors, they agreed with the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [the original article was published in Oncology Reports 34 2202‑2210, 2015; DOI 10.3892/or.2015.4165].