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The antineoplastic effects of 5‐hydroxytryptamine (5‐HT) receptor antagonists have been shown in previous studies. However, the exact underlying mechanisms mediating these antineoplastic effects are unclear. In the present study, we assessed the antineoplastic effects of tropisetron, a 5‐HT receptor antagonist, in an experimental model of lung cancer in BALB/c mouse. Lewis lung carcinoma cell line was used to induce lung cancer. Mice were divided into four groups (n = 6) as follows: tumor‐bearing mice + tropisetron (5 mg/kg intraperitoneally [IP]), tumor‐bearing mice + tropisetron (10 mg/kg IP), tumor‐bearing mice + saline, healthy mice + tropisetron (10 mg/kg). Tumor burden, interferon‐γ (IFN‐γ), interleukin (IL)‐4, pathological response, Ki‐67, and E‐cadherin were assessed using enzyme‐linked immunosorbent assay, and real‐time polymerase chain reaction. Comet assay was used to assess DNA toxicity. Tropisetrone‐treated animals (either 5 or 10 mg/kg) showed significantly lower tumor sizes at the day 24th after tumor induction. Tropisetron received animals also showed significantly higher levels of IFN‐γ, E‐cadherin, pathologic response, and necrotic cells compared to the saline‐treated counterparts. In addition, the levels of IL‐4, and Ki‐67 were significantly lower in tropisetrone treated mice in comparison with control. Furthermore, tropisteron coadministration signifcantly reduced H2O2‐induced DNA toxicity while treatment with tropisteron alone showed no adverse effect on DNA. Tropisetrone can be used as a potential antineoplastic drug in lung cancer. This agent can promote its antineoplastic effects in part through modulating inflammatory and proliferating markers.