Role of myeloid-derived suppressor cells in metastasis

Cole, Kathryn; Pravoverov, Kristina; Talmadge, James E.

doi:10.1007/s10555-020-09947-x

Cited by 26 publications

(19 citation statements)

References 204 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The immunity-sparing LRP, as compared to ORP, is potentially advantageous in terms of not upregulating MDSCs capable of provoking dormant tumors. An increasing body of evidence demonstrates that immunosuppressive mechanisms mediated by MDSCs are a key contributor to tumor progression and that these mechanisms promote tumor escape from dormancy [16]. The potential LRP benefit of preventing surgery-induced MDSC upregulation did not result in better treatment outcomes in our study participants.…”

Section: Discussionmentioning

confidence: 63%

See 1 more Smart Citation

Immunophenotype Rearrangement in Response to Tumor Excision May Be Related to the Risk of Biochemical Recurrence in Prostate Cancer Patients

Bosas

Zaleskis

Dabkevičienė

et al. 2021

JCM

View full text Add to dashboard Cite

Background: Prostate cancer (PCa) is known to exhibit a wide spectrum of aggressiveness and relatively high immunogenicity. The aim of this study was to examine the effect of tumor excision on immunophenotype rearrangements in peripheral blood and to elucidate if it is associated with biochemical recurrence (BCR) in high risk (HR) and low risk (LR) patients. Methods: Radical prostatectomy (RP) was performed on 108 PCa stage pT2–pT3 patients. Preoperative vs. postoperative (one and three months) immunophenotype profile (T- and B-cell subsets, MDSC, NK, and T reg populations) was compared in peripheral blood of LR and HR groups. Results: The BCR-free survival difference was significant between the HR and LR groups. Postoperative PSA decay rate, defined as ePSA, was significantly slower in the HR group and predicted BCR at cut-off level ePSA = −2.0% d−1 (AUC = 0.85 (95% CI, 0.78–0.90). Three months following tumor excision, the LR group exhibited a recovery of natural killer CD3 − CD16+ CD56+ cells, from 232 cells/µL to 317 cells/µL (p < 0.05), which was not detectable in the HR group. Prostatectomy also resulted in an increased CD8+ population in the LR group, mostly due to CD8+ CD69+ compartment (from 186 cells/µL before surgery to 196 cells/µL three months after, p < 001). The CD8+ CD69+ subset increase without total T cell increase was present in the HR group (p < 0.001). Tumor excision resulted in a myeloid-derived suppressor cell (MDSC) number increase from 12.4 cells/µL to 16.2 cells/µL in the HR group, and no change was detectable in LR patients (p = 0.12). An immune signature of postoperative recovery was more likely to occur in patients undergoing laparoscopic radical prostatectomy (LRP). Open RP (ORP) was associated with increased MDSC numbers (p = 0.002), whereas LRP was characterized by an immunity sparing profile, with no change in MDSC subset (p = 0.16). Conclusion: Tumor excision in prostate cancer patients results in two distinct patterns of immunophenotype rearrangement. The low-risk group is highly responsive, revealing postoperative restoration of T cells, NK cells, and CD8+ CD69+ numbers and the absence of suppressor MDSC increase. The high-risk group presented a limited response, accompanied by a suppressor MDSC increase and CD8+ CD69+ increase. The laparoscopic approach, unlike ORP, did not result in an MDSC increase in the postoperative period.

show abstract

Section: Discussionmentioning

confidence: 63%

“…Many cancers, including PCa, are known to elicit an overproduction of a range of immunocyte suppressors, including immature myeloid cells, which recently were categorized as myeloid-derived suppressor cells (MDSCs) [14][15][16][17]. Tumor excision response of MDSC in PCa patients has also been reported [15].…”

Section: Introductionmentioning

confidence: 99%

Immunophenotype Rearrangement in Response to Tumor Excision May Be Related to the Risk of Biochemical Recurrence in Prostate Cancer Patients

Bosas

Zaleskis

Dabkevičienė

et al. 2021

JCM

View full text Add to dashboard Cite

show abstract

“…Notably, MDSCs play a crucial role in tumor escape, angiogenesis, and metastasis [19,20]. In metastasis, the tumor cells require a favorable environment for growth and dissemination to nearby organs and tissues [21]. Accordingly, MDSCs enhance metastasis by forming the pre-metastatic niches to promote circulating tumor cells [22].…”

Section: Myeloid-derived Suppressor Cells (Mdscs)mentioning

confidence: 99%

Targeting Tumor Microenvironment-associated Immune Cells with Nanoparticles-based Strategies

Alotaibi¹

2021

Pharmacophore

View full text Add to dashboard Cite

The propensity of cancer cells to escape the immune system and to initiate a complex balance environment is due to its ability to utilize immune cells via associated factors, including non-tumoral components such as blood vessels, fibroblasts, cells, and signaling molecules. Collectively, these are referred to as the tumor microenvironment (TME). TME is the tumor's surrounding environment and has a crucial role in promoting tumor progression, angiogenesis, metastasis, and increasing tumor resistance to several therapies. TME's immunosuppressive factors depress the immune response after altering the metabolism of immune cells within TME. Accordingly, targeting TME with nanoparticles may be a beneficial tool to regulate and enhance the efficacy of tumor immunotherapies. Here, we review distinct structural and functional properties of immune cells within TME, tumor-associated immunosuppressive factors, and the interaction between TME and immune cells. We finish with a summary of recent findings related to novel nanoparticle strategies to target TME.

show abstract

“…Inhibition of angiogenesis is associated with alleviation of cancer progression and metastasis [4,5]. New blood vessels formed during angiogenesis may contribute to inflammation-associated carcinogenesis, inducing tumor progression and tumor metastasis [6,7]. Unregulated release of different inflammatory mediators in the tumor microenvironment (TME) activates growth, proliferation, and migration of colorectal cancer cells [8].…”

Section: Introductionmentioning

confidence: 99%

An Aptamer-Based Antagonist against the Receptor for Advanced Glycation End-Products (RAGE) Blocks Development of Colorectal Cancer

Zheng

Zhu

et al. 2021

Mediators of Inflammation

View full text Add to dashboard Cite

Tumor angiogenesis plays a crucial role in colorectal cancer development. Dysregulation of the receptor for the advanced glycation end-products (RAGE) transmembrane signaling mediates inflammation, resulting in various cancers. However, the mechanism of the RAGE signaling pathway in modulating development of colorectal cancer has not been explored. In this study, an aptamer-based RAGE antagonist (Apt-RAGE) was used to inhibit interaction between RAGE and S100B, thus blocking downstream NFκB-mediated signal transduction. In vitro results showed that Apt-RAGE effectively inhibited S100B-dependent and S100B-independent RAGE/NFκB activation in colorectal HCT116 cancer cells, thus decreasing proliferation and migration of cells. Notably, expression and secretion of VEGF-A were inhibited, implying that Apt-RAGE can be used as an antiangiogenesis agent in tumor therapy. Moreover, Apt-RAGE inhibited tumor growth and microvasculature formation in colorectal tumor-bearing mice. Inhibition of angiogenesis by Apt-RAGE was positively correlated with suppression of the RAGE/NFκB/VEGF-A signaling. The findings of this study show that Apt-RAGE antagonist is a potential therapeutic agent for treatment of colorectal cancer.

show abstract

Role of myeloid-derived suppressor cells in metastasis

Cited by 26 publications

References 204 publications

Immunophenotype Rearrangement in Response to Tumor Excision May Be Related to the Risk of Biochemical Recurrence in Prostate Cancer Patients

Immunophenotype Rearrangement in Response to Tumor Excision May Be Related to the Risk of Biochemical Recurrence in Prostate Cancer Patients

Targeting Tumor Microenvironment-associated Immune Cells with Nanoparticles-based Strategies

An Aptamer-Based Antagonist against the Receptor for Advanced Glycation End-Products (RAGE) Blocks Development of Colorectal Cancer

Contact Info

Product

Resources

About