Significance of TIM-3 expression by CD4+ and CD8+ T lymphocytes in tumor-draining lymph nodes from patients with breast cancer

Shariati, Sahar; Ghods, Atri; Zohouri, Mahshid; Rasolmali, Reza; Talei, Abdolrasoul; Mehdipour, Fereshteh; Ghaderi, Abbas

doi:10.1016/j.molimm.2020.10.002

Cited by 11 publications

(7 citation statements)

References 34 publications

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“…Cell migration lies in the high affinity and absolute specificity of CXCR4 for its ligand SDF, namely, CXCR4 is the only receptor for SDF. Studies show that the impact of the SDF-1/CXCR4 biological axis on tumors is multifaceted and playing an important role in the occurrence, development and metastasis of multiple tumors (25)(26)(27)(28)(29)(30).…”

Section: Discussionmentioning

confidence: 99%

The mechanism of LncRNA01977 in lung adenocarcinoma through the SDF-1/CXCR4 pathway

Lai¹,

Wang²,

Qin³

2022

Transl Cancer Res TCR

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Background: A significant correlation has been identified between lncRNA and tumor cell resistance, diagnosis, and prognosis. Although mRNA studies have dominated the field of non-coding RNA biology in tumorigenesis in recent years, long-chain non-coding RNA (the biological function) has also attracted increasing attention. However, the lncRNA associated with lung adenocarcinoma (LUAD) remains unexplored. This study used bioinformatics analysis to screen and identify LncRNA01977 as a key oncogenic driver of LUAD. Methods:The experiment was divided into blank serum group (normal serum medium) and lung compound low, medium and high dose groups (5%, 10%, 15% and 15% lung compound drug serum medium, respectively). Transwell invasion ability of A549 cells was detected, and Western blot tested A549 cells SDF-1 specific receptor CXCR4, and CXCR4 gene expression in A549 cells were determined by reverse transcription-polymerase chain reaction (RT-PCR). In addition, western blotting, MTT proliferation test, colony formation test and apoptosis detection techniques were used to explore the mechanism of LncRNA01977's effects on LUAD.Results: In vitro assays demonstrated that LncRNA01977 can significantly promote the progression of LUAD and that stromal cells in tumor microenvironment secrete chemokine CXCL12, also known as stromal derived factor-1 (SDF-1), and its receptor CXCR4 is low expressed in normal tissues and high expressed in LUAD tissues. Lung cancer patients with high expression of CXCR4 are more prone to metastasis.Conclusions: LncRNA01977 can be used as a new prognostic indicator of LUAD, and can help patients to find more effective target treatment options for LUAD.

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Section: Discussionmentioning

confidence: 99%

The mechanism of LncRNA01977 in lung adenocarcinoma through the SDF-1/CXCR4 pathway

Lai¹,

Wang²,

Qin³

2022

Transl Cancer Res TCR

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“…TIM3 expression represented dysfunctional tumor in ltrating CD8 + T cells in renal cell carcinoma [30,15]. TIM3 expression was related to poor prognosis of tumors [31,32,33]. Anti-TIM3 antibody promoted T cell IFN-mediated anti-tumor immunity and suppresses tumors [34].…”

Section: Discussionmentioning

confidence: 99%

PAX5 Haploinsufficiency Induces Immune Inhibitory-Related Molecules Expressions of CD8 + T Cells in the Tumor Microenvironment

Gong

Wang

et al. 2021

Preprint

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Loss of function of PAX5 plays an important role in PAX5 mutation tumor, and PAX5 haploinsufficiency promoting tumorigenesis is related to immune escape. But the mechanisms of PAX5 mutations inducing tumor immune escape have not been clarified. We estimated the proportions of 22 immune cell types and the expressions of immune inhibitory-related molecules based on gene expression profiles (GEPs) from B- acute lymphoblastic leukemia(B-ALL) with PAX5 mutations by CIBERSORT, an established algorithm. We constructed the PAX5 haplodeletion A20 cell lines, built allografted A20 tumor models and evaluated the effect of PAX5 haplodeletion on immune inhibitory-related molecules in the tumor microenvironment (TME). Our results indicated the percentages of T cells in bone marrow of B-ALL with PAX5 mutations were not statistically different from that in bone marrow of B-ALL without PAX5 mutations, except for T follicular helper (Tfh) cells. But a variety of up-regulated immune inhibitory-related molecules in bone marrow of B- ALL with PAX5 mutations were identified. By different approaches, we found that several immune inhibitory-related molecules of CD8+ T cells in TME of PAX5 haplodeletion clones such as TIM3, NR4A1 and BATF, were increased significantly compared with that of PAX5 wild type control. The IFN-ɤ of CD8+ T cells in TME of PAX5 haplodeletion tumors was decreased significantly compared with that of PAX5 wild type control. Our study showed that PAX5 haploinsufficiency induced high expressions of TIM3, NR4A1 and BATF in the TME and was involved in CD8+ T cells dysfunction or exhaustion.

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“…Another study assessed the association of Tim-3 expression on T cells from tumor-draining lymph nodes with breast cancer progression. The authors reported that the frequency of Tim-3 + CD8 + T cells was associated with a higher tumor grade and was significantly higher in patients with more involved lymph nodes than in those with fewer involved nodes ( 37 ). The underlying mechanism for this could be the Tim-3-mediated inhibition of the proliferation and activation of CD8 + T cells.…”

Section: The Role Of Tim-3 Expression On Immune Cells In Breast Cancermentioning

confidence: 99%

“…The expression of Tim-3 in CD4 + T cells was also upregulated in breast cancer ( 28 ), and correlated with metastatic lymph node load ( 37 ), suggesting its importance in suppressing the immune microenvironment. The Tim-3 level in circulating Tfh (CD4 + CXCL13 + follicular helper T) cells in patients with breast cancer was significantly elevated, which was a Tfh exhaustion marker.…”

Section: The Role Of Tim-3 Expression On Immune Cells In Breast Cancermentioning

confidence: 99%

The Emerging Role of T-Cell Immunoglobulin Mucin-3 in Breast Cancer: A Promising Target For Immunotherapy

et al. 2021

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Cancer treatment through immune checkpoint receptor blockade has made significant advances in the recent years. However, resistance to the current immune checkpoint inhibitors (ICIs) has been observed in many patients, who consequently do not respond to these treatments. T-cell immunoglobulin mucin-3 (Tim-3) is a novel immune checkpoint molecule emerging as a potential therapeutic target for cancer immunotherapy. Epidemiologic findings reveal that genetic polymorphisms in the Tim-3 gene are associated with increased susceptibility to breast cancer. In patients with breast cancer, Tim-3 is expressed both on immune and tumor cells. Accumulating evidence demonstrates that Tim-3 can notably affect breast cancer treatment outcome and prognosis. Therefore, Tim-3 is being regarded as a high-potential target for improving breast cancer therapy. In this review, we summarize the role of Tim-3 in breast cancer and the regulation mechanisms of Tim-3 to furnish evidences for future research and therapy.

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Significance of TIM-3 expression by CD4+ and CD8+ T lymphocytes in tumor-draining lymph nodes from patients with breast cancer

Cited by 11 publications

References 34 publications

The mechanism of LncRNA01977 in lung adenocarcinoma through the SDF-1/CXCR4 pathway

The mechanism of LncRNA01977 in lung adenocarcinoma through the SDF-1/CXCR4 pathway

PAX5 Haploinsufficiency Induces Immune Inhibitory-Related Molecules Expressions of CD8 + T Cells in the Tumor Microenvironment

The Emerging Role of T-Cell Immunoglobulin Mucin-3 in Breast Cancer: A Promising Target For Immunotherapy

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