Green tea catechins, in particular, have attracted attention as cancer‑preventive agents due to their low toxicity and ready availability to the general population, as well as exerting preventive effects against cancers in humans (2‑5). A prospective cohort study on a Japanese population demonstrated that green tea has a strong potency in preventing cancers in a variety of organs (6). Additional epidemiological or clinical studies revealed that green tea consumption is inversely associated with the progression of prostate cancer, the risk of hematological malignancies and the risk of breast cancer recurrence, among others (7‑9). In cells cultured for in vitro experiments on green tea catechins, growth inhibition and apoptosis induction have been observed in a variety of cell lines (10,11). Previously, using two cell lines, peripheralblood T lymphocytes of adult T‑cell leukemia patients and human T‑cell leukemia virus type 1 (HTLV‑1)‑infected T‑cell line, it was demonstrated that EGCg inhibited cell growth concomitant with the induction of apoptosis, and was responsible for suppressing the expression of HTLV‑1 pX mRNA, which encodes the oncoprotein, Tax (12). Tax protein plays an important role in HTLV‑1‑infected T‑cell leukemogenesis by mediating interactions with transcription factors, including nuclear factor (NF)‑κB. In the CTLL‑2 Tax‑expressing mouse T‑cell line, constitutive expression of B‑cell lymphoma‑extra large (Bcl‑xL) via the NF‑κB pathway has been shown to contribute to the inhibition of apoptosis (13).