Waterpipe tobacco smoking (WPS) continues to spread globally and presents serious health hazards. The aim of the present study was to investigate the effects of treatment with WPS condensate (WPSC) on lung cell proliferation and plasticity as well as tumor cell recognition and killing by natural killer (NK) cells using cytotoxicity assays. The results indicated that exposure of normal and cancer lung cell lines to WPSC resulted in a decrease in their in vitro growth in a dose-dependent manner and it induced tumor senescence. Selleck Ribociclib In addition, WPSC selectively caused DNA damage as revealed by an increase in γH2AX and 53BP1 in tumor lung cells. To gain further insight into the molecular mechanisms altered by WPSC, we conducted a global comprehensive transcriptome analysis of WPSC-treated tumor cells. Data analysis identified an expression profile of genes that best distinguished treated and non-treated cells involving several pathways. Of these pathways, we focused on those involved in epithelial to mesenchymal transition (EMT) and stemness. Results showed that WPSC induced an increase in SNAI2 expression associated with EMT, ACTA2 and SERPINE2 were involved in invasion and CD44 was associated with stemness. Furthermore, WPSC exposure increased the expression of inflammatory response genes including CASP1, IL1B, IL6 and CCL2. While immune synapse formation between NK and WPSC-treated lung cancer target cells was not affected, the capacity of NK cells to kill these target cells was reduced. The data reported in the present study are, to the best of our knowledge, the first in vitro demonstration of WPSC effects on lung cellular parameters providing evidence of its potential involvement in tumor physiology and development.External and internal stimuli are often involved in the pathogenesis of tumors, and the deterioration of endoplasmic reticulum (ER) function within cells is also an important etiological factor of tumorigenesis resulting in the impairment of the endoplasmic reticulum, which is termed ER stress. The ER is an organelle that serves a crucial role in the process of protein synthesis and maturation, and also acts as a reservoir of calcium to maintain intracellular Ca2+ homeostasis. ER stress has been revealed to serve a critical role in tumorigenesis. In the present review, the association between ER stress‑related pathways and tumor cell apoptosis is examined. Primarily, the role of ER stress in tumor cell apoptosis is discussed, and it is stipulated that ER stress, induced by drugs both directly and indirectly, promotes tumor cell apoptosis.Non‑small cell lung cancer (NSCLC) is the leading cause of cancer‑related deaths worldwide. Cisplatin‑based chemotherapy currently represents the main treatment option for patients with NSCLC. The aim of the present study was to evaluate effect of single nucleotide polymorphisms (SNPs) within the excision repair cross‑complementing group 5 (ERCC5) gene on susceptibility to NSCLC, as well as the responsiveness to and toxicity of cisplatin chemotherapy. A total of 506 patients with NSCLC and 510 healthy controls were recruited for the present study. All DNA samples were genotyped by the Agena MassARRAY platform. Logistic regression analysis was carried out to assess the relationship between ERCC5 polymorphisms with NSCLC susceptibility and responsiveness to chemotherapy. The rs4771436 TG‑GG genotype was associated with increased NSCLC risk. When the data were stratified according to age, sex, tobacco smoking, body mass index and histological type, ERCC5 polymorphisms (rs2016073, rs4771436, rs11069498 and rs4150330) were associated with NSCLC risk. Furthermore, the A allele and GA‑AA genotype of rs11069498 were related to the response to chemotherapy. ERCC5 (rs11069498 and rs4150330) polymorphisms were associated with the increased risk of toxicity. However, rs4771436 in ERCC5 gene was significantly correlated with the reduced risk of toxicity. These results suggested a potential relationship between ERCC5 polymorphisms, the risk of NSCLC and the sensitivity to cisplatin‑based chemotherapy among Chinese populations.Non‑Hodgkin lymphoma (NHL) is a form of lymphoid malignancy, with diffuse large B cell lymphoma (DLBCL) being the most common NHL isoform. Approximately half of patients with DLBCL are successfully cured via first‑line Rituximab, Cyclophosphamide, Epirubicin, Vindesine, Prednisolone (R‑CHOP) treatment. However, 30‑40% of patients with DLBCL ultimately suffer from treatment‑refractory or relapsed disease. These patients often suffer from high mortality rates owing to a lack of suitable therapeutic options, and all patients are at a high risk of serious treatment‑associated dose‑dependent toxicity. As such, it is essential to develop novel treatments for NHL that are less toxic and more efficacious. Oncolytic Vaccinia virus (OVV) has shown promise as a means of treating numerous types of cancer. Gene therapy strategies further enhance OVV‑based therapy by improving tumor cell recognition and immune evasion. Beclin1 is an autophagy‑associated gene that, when upregulated, induces excess autophagy and cell death. The present study aimed to develop an OVV‑Beclin1 therapy capable of inducing autophagic tumor cell death. OVV‑Beclin1 was able to efficiently kill NHL cells and to increase the sensitivity of these cells to R‑CHOP, thereby decreasing the dose‑dependent toxic side effects associated with this chemotherapeutic regimen. The combination of OVV‑Beclin1 and R‑CHOP also significantly improved tumor growth inhibition and survival in a BALB/c murine model system owing to the synergistic induction of autophagic cell death. Together, these findings suggest that OVV‑Beclin1 infection can induce significant autophagic cell death in NHL, highlighting this as a novel means of inducing tumor cell death via a mechanism that is distinct from apoptosis and necrosis.Emerging evidence has indicated that histone modification and its related regulators are involved in the progression of multiple myeloma (MM) cells. In the present study, the expression of Jumonji C domain‑containing 2 (JMJD2) was examined in both MM tissues and healthy controls. The roles of JMJD2C in the progression of MM were further investigated. The results revealed that the expression of JMJD2C, but not that of JMJD2A or JMJD2B, was increased in MM tissues compared with the healthy controls. The overexpression of JMJD2C significantly increased the in vitro growth of MM cells. The inhibitor of the β‑catenin signaling pathway significantly attenuated the JMJD2C‑induced growth of MM cells. Mechanistical analyses indicated that JMJD2C increased the transcription of β‑catenin in MM cells, which may be due to the fact that JMJD2C can directly bind with the promoter of β‑catenin. Furthermore, JMJD2C activated β‑catenin in MM cells via a GSK3β‑dependent manner, which was evidenced by the results demonstrating that the overexpression of GSK3β attenuated the JMJD2C‑induced decrease in the phosphorylation of β‑catenin.