Intracellular Mechanisms of Tumor Cell Immunoresistance

Hermanowicz, Justyna Magdalena; Sieklucka, Beata; Nosek, Krzysztof; Pawlak, Dariusz

doi:10.18388/abp.2020_2878

Cited by 3 publications

(2 citation statements)

References 56 publications

(64 reference statements)

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“…In order to explore the anti-tumor mechanism, we detect the expression of related protein and found that maprotiline inhibits the expression of PD-L1. Blocking the link of PD-1 and PD-L1 could recover the T cell function to destroy tumor cells [25]. It is might a reason that maprotiline delays the growth of melanoma.…”

Section: Discussionmentioning

confidence: 99%

Maprotiline Prompt the Anti-tumor Effect by Inhibiting the PD-L1 in Mice Burdened Melanoma

Zhao

Yang

Liu

et al. 2021

Preprint

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Programmed cell death 1 ligand 1(PD-L1) binds with programmed cell death protein 1 (PD-1) to inhibit the responses of T cells. PD-L1 is significantly upregulated on tumor cells and blocking the PD-L1/PD-1 signal has become an important target of immunotherapy in clinic. At present, some old drugs of non-antitumor have been found that could play the effect of anti-tumor. Maprotiline, as a tetracyclic antidepressant, has been widely used for treating mental depression. Here, we study the anti-tumor effect of maprotiline by strengthening the immune response of mice. In vitro, treatment with maprotiline inhibits the proliferation and migration of B16 cells, increases the cell apoptosis. Importantly, treatment with maprotiline reduces the expression of PD-L1 in tumor tissue, prompts the ratios of CD4+ T cells, CD8+ T cells and NK cells in spleens, increases the infiltration of CD4+ and CD8+ T cells in tumor-tissues. In brief, we determine that maprotiline could prompt the anti-tumor immune response by inhibiting the PD-L1 in mice. This study may find a new inhibitor of PD-L1, which provides a new drug treated tumor in clinical.

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Section: Discussionmentioning

confidence: 99%

Maprotiline Prompt the Anti-tumor Effect by Inhibiting the PD-L1 in Mice Burdened Melanoma

Zhao

Yang

Liu

et al. 2021

Preprint

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“…This ligand, after binding to its receptor PD-1 (programmed cell death protein 1) on immune cells, exerts multiple effects on them. Enhanced conversion of CD4+ Tcells into immunosuppressive Treg, decreased cytotoxicity of CD8+ Tcells, reprogramming macrophages into M2 subtypes, which inhibit immunity, are among well-studied effects acquired after PD-L1/PD-1 pathway activation [4,5]. The third and the most complex mechanism triggered by cancer cells for immune evasion is the excretion of prosurvival factors and molecules, which enable the production of an immunosuppressive microenvironment.…”

Section: Mechanisms Involved In Immune Evasionmentioning

confidence: 99%

Not Only Immune Escape—The Confusing Role of the TRP Metabolic Pathway in Carcinogenesis

Kwiatkowska

Hermanowicz

Przybyszewska-Podstawka

et al. 2021

Cancers

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Background: The recently discovered phenomenon that cancer cells can avoid immune response has gained scientists' interest. One of the pathways involved in this process is tryptophan (TRP) metabolism through the kynurenine pathway (KP). Individual components involved in TRP conversion seem to contribute to cancerogenesis both through a direct impact on cancer cells and the modulation of immune cell functionality. Due to this fact, this pathway may serve as a target for immunotherapy and attempts are being made to create novel compounds effective in cancer treatment. However, the results obtained from clinical trials are not satisfactory, which raises questions about the exact role of KP elements in tumorigenesis. An increasing number of experiments reveal that TRP metabolites may either be tumor promoters and suppressors and this is why further research in this field is highly needed. The aim of this study is to present KP as a modulator of cancer development through multiple mechanisms and to point to its ambiguity, which may be a reason for failures in treatment based on the inhibition of tryptophan metabolism

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Investigating the immune mechanism of natural products in the treatment of lung cancer

Yang,

Chen,

Liu

et al. 2024

Front. Pharmacol.

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With the deepening of people’s understanding of lung cancer, the research of lung cancer immunotherapy has gradually become the focus of attention. As we all know, the treatment of many diseases relies on the rich sources, complex and varied compositions and wide range of unique biological properties of natural products. Studies have shown that natural products can exert anticancer effects by inducing tumor cell death, inhibiting tumor cell proliferation, and enhancing tumor cell autophagy. More notably, natural products can adjust and strengthen the body’s immune response, which includes enhancing the function of NK cells and promoting the differentiation and proliferation of T lymphocytes. In addition, these natural products may enhance their anticancer effects by affecting inhibitory factors in the immune system, hormone levels, enzymes involved in biotransformation, and modulating other factors in the tumor microenvironment. The importance of natural products in lung cancer immunotherapy should not be underestimated. However, the specific links and correlations between natural products and lung cancer immunity are not clear enough, and further studies are urgently needed to clarify the relationship between the two. In this paper, we will focus on the correlation between natural products and lung cancer immune responses, with a view to providing new research perspectives for immunotherapy of lung cancer.

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Intracellular Mechanisms of Tumor Cell Immunoresistance

Cited by 3 publications

References 56 publications

Maprotiline Prompt the Anti-tumor Effect by Inhibiting the PD-L1 in Mice Burdened Melanoma

Maprotiline Prompt the Anti-tumor Effect by Inhibiting the PD-L1 in Mice Burdened Melanoma

Not Only Immune Escape—The Confusing Role of the TRP Metabolic Pathway in Carcinogenesis

Investigating the immune mechanism of natural products in the treatment of lung cancer

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