Mechanism and clinical application of thymosin in the treatment of lung cancer

Abstract

Cancer is one of the leading causes of death worldwide. The burden of cancer on public health is becoming more widely acknowledged. Lung cancer has one of the highest incidence and mortality rates of all cancers. The prevalence of early screening, the emergence of targeted therapy, and the development of immunotherapy have all significantly improved the overall prognosis of lung cancer patients. The current state of affairs, however, is not encouraging, and there are issues like poor treatment outcomes for some patients and extremely poor prognoses for those with advanced lung cancer. Because of their potent immunomodulatory capabilities, thymosin drugs are frequently used in the treatment of tumors. The effectiveness of thymosin drugs in the treatment of lung cancer has been demonstrated in numerous studies, which amply demonstrates the potential and future of thymosin drugs for the treatment of lung cancer. The clinical research on thymosin peptide drugs in lung cancer and the basic research on the mechanism of thymosin drugs in anti-lung cancer are both systematically summarized and analyzed in this paper, along with future research directions.

Keywords: immunotherapy; lung cancer; therapy; thymalfasin; thymopentin; thymosin; thymosin alpha 1.

Figure 1

The summary of clinical research and the basic research on the mechanism of thymosin drugs in anti-lung cancer.

Figure 2

The effects of thymosin monotherapy and combination therapy (with chemotherapeutic drugs, IFN or IL-2) on the treatment of lung cancer Thymosin monotherapy and combination therapy inhibit the growth, proliferation, invasion, migration, carcinogenesis, and antioxidant activity of lung cancer. Thymosin plus IFN and IL-2 exert positive immunomodulatory effects on T lymphocyte by upregulating CD8⁺ T cell levels, increasing T cell activation, and enhancing the immune response of T lymphocytes. Thymosin restores the activity of NK cells, enhances the effectiveness of chemotherapeutic drugs. IFN, interferon; IL-2, interleukin-2; NK, natural killer. The figure is partly generated using Servier Medical Art provided by Servier, licensed under a Creative Commons Attribution 3.0 Unported License.

Figure 3

The major mechanism of thymosin in the treatment of lung cancer By upregulating IFN-γ and CD86, as well as inhibiting CD31, thymosin inhibited the growth of LCLC/LUAD and boosted the immune response of T lymphocytes. Thymosin inhibited the proliferation, migration, and antioxidant activity of LC by inhibiting the expression of ROS, upregulating catalase, peroxide dismutase, and glutathione peroxidase. Thymosin increased CD8⁺ T cell levels, inhibited the growth of LUAD. Thymosin inhibited the invasion and migration of LC by inhibiting STAT3 and then MMP2. ROS, reactive oxygen species; IFN-γ, interferon-γ; STAT3, signal transducer and activator of transcription 3; MMP2, matrix metalloproteinase 2; LCLC, large cell lung cancer; LUAD, lung adenocarcinoma; LC, lung cancer. The figure is partly generated using Servier Medical Art provided by Servier, licensed under a Creative Commons Attribution 3.0 Unported License.