Lymphoma is a type of cancer that develops from certain immune system cells. Arsenic trioxide (ATO) has attracted wide attention owing to its antitumor activities. However, the role of ATO in tumorigenesis and progression remains to be investigated. In the present study, the antitumor function of ATO was investigated in in lymphoma Raji and Jurkat cell lines and the effect of ATO on nuclear factor (NF)-κB expression levels. A Cell Counting kit-8 assay was used to assess cellular proliferation and the degree of cell apoptosis was measured by flow cytometric analysis; these assays demonstrated that ATO inhibited proliferation and promoted the apoptosis of Raji and Jurkat cells in a dose- and time-dependent manner. Western blot analysis revealed that ATO treatment affected the expression of apoptosis-associated proteins by downregulating the anti-apoptotic protein B-cell lymphoma-2 (Bcl-2) and upregulating the pro-apoptotic protein Bcl-2-associatedX and the degree of caspase-3 cleavage. In addition, reverse transcription-quantitative polymerase chain reaction and western blot analysis showed that the mRNA and protein expression levels of NF-κB were downregulated significantly following treatment with 2 µM ATO for 24, 48 and 72 h in the two cell lines. Additionally, immunofluorescence staining indicated that NF-κB expression diminished following ATO treatment in a time-dependent manner. These data indicated that ATO inhibited the proliferation of lymphoma cells by inducing cell apoptosis, which may be associated with the inhibition of the NF-κB signaling pathway. The findings of the present study may lay the foundation for developing a personalized medicine strategy using ATO via targeting of the NF-κB signaling pathway in lymphoma.

Lung cancer has the highest incidence and mortality rate worldwide among all malignancy-associated mortalities, of which non-small cell lung cancer accounts for 80% of all cases. Resistance against epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) develops following 8-12 months of disease progression, and is a critical issue. HCC827 cell lines with resistance to EGFR-TKIs were successfully screened. The half maximal inhibitory concentration values were 1,000-fold higher than the values for the parental HCC827 cell line, thereby demonstrating cross-resistance against the same family of TKIs. The expression of B-cell lymphoma 2 (Bcl2) was markedly increased in the resistant clones, as well as in the patient biopsies. The phosphatase and tensin homolog phosphoinositide 3-kinase signaling axis is a potential mechanism for acquiring resistance, and therefore targeting Bcl2 may be a useful strategy for further investigations.