Abstract
Tumor necrosis factor receptor 2 (TNFR2) is expressed on some tumor cells, such as myeloma, Hodgkin lymphoma, colon cancer and ovarian cancer, as well as immunosuppressive cells. There is increasingly evidence that TNFR2 expression in cancer microenvironment has significant implications in cancer progression, metastasis and immune evasion. Although nanomedicine has been extensively studied as a carrier of cancer immunotherapeutic agents, no study to date has investigated TNFR2-targeting nanomedicine in cancer treatment. From an epigenetic perspective, previous studies indicate that DNA demethylation might be responsible for high expressions of TNFR2 in cancer models. This perspective review discusses a novel therapeutic strategy based on nanomedicine that has the capacity to target TNFR2 along with inhibition of DNA demethylation. This approach may maximize the anti-cancer potential of nanomedicine-based immunotherapy and, consequently, markedly improve the outcomes of the management of patients with malignancy.
Highlights
Tumor necrosis factor (TNF) was first described in the early 1960s as its originally discovered role during tumor regression in rodents [1]
The samples were subjected membrane protein expression arrays, ELISAs and few other assays that are related to the functional of Tumor necrosis factor receptor 2 (TNFR2) target
It is known that the TNF works as an anti-tumor cytokine, while its role may be negatively converted to be a tumor-promoting substance upon its conjugation with TNFR2, which is only expressed on some tumor cells and immunosuppressive cells
Summary
Tumor necrosis factor (TNF) was first described in the early 1960s as its originally discovered role during tumor regression in rodents [1]. As inflammation plays a key role in cancer progression and the microenvironment of cancer is controlled by inflammatory cells [4], previous studies have explored TNF-TNFRs interactions in cancer proliferation, metastasis and immune evasion [5]. These studies concluded that TNF works as a tumor-suppressive cytokine through interaction with TNFR1, which is expressed on both normal. MRNA nor protein detection has made it difficult to study these cell subsets in the context of various diseases To bypass this problem, previous studies have used DNA demethylation within the FOXP3 gene, to identify Tregs in human peripheral tissue. To improve the efficiency of cancer immunotherapy, we hypothesized that using DNA demethylation inhibitor along with nanomedicine targeting TNFR2 could be a novel effective approach towards cancer therapy
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