Modulating the tumor immune microenvironment with nanoparticles: A sword for improving the efficiency of ovarian cancer immunotherapy

Xu, Tianyue; Liu, Zhihui; Huang, Liwen; Jing, Jing; Liu, Xiaowei

doi:10.3389/fimmu.2022.1057850

Cited by 7 publications

(8 citation statements)

References 177 publications

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“…S8 ). Enhanced immunogenicity in tumor tissues should lead to more immunocyte infiltration as well as activation, thereby driving an antitumor immune response 33 .…”

Section: Resultsmentioning

confidence: 99%

B-Myb deficiency boosts bortezomib-induced immunogenic cell death in colorectal cancer

Hui,

Yu,

et al. 2024

Sci Rep

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B-Myb has received considerable attention for its critical tumorigenic function of supporting DNA repair. However, its modulatory effects on chemotherapy and immunotherapy have rarely been reported in colorectal cancer. Bortezomib (BTZ) is a novel compound with chemotherapeutic and immunotherapeutic effects, but it fails to work in colorectal cancer with high B-Myb expression. The present study was designed to investigate whether B-Myb deletion in colorectal cancer could potentiate the immune efficacy of BTZ against colorectal cancer and to clarify the underlying mechanism. Stable B-Myb knockdown was induced in colorectal cancer cells, which increased apoptosis of the cancer cells relative to the control group in vitro and in vivo. We found that BTZ exhibited more favourable efficacy in B-Myb–defective colorectal cancer cells and tumor-bearing mice. BTZ treatment led to differential expression of genes enriched in the p53 signaling pathway promoted more powerful downstream DNA damage, and arrested cell cycle in B-Myb–defective colorectal cancer. In contrast, recovery of B-Myb in B-Myb–defective colorectal cancer cells abated BTZ-related DNA damage, cell cycle arrest, and anticancer efficacy. Moreover, BTZ promoted DNA damage–associated enhancement of immunogenicity, as indicated by potentiated expression of HMGB1 and HSP90 in B-Myb–defective cells, thereby driving M1 polarization of macrophages. Collectively, B-Myb deletion in colorectal cancer facilitates the immunogenic death of cancer cells, thereby further promoting the immune efficacy of BTZ by amplifying DNA damage. The present work provides an effective molecular target for colorectal cancer immunotherapy with BTZ.

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“…S8 ). Enhanced immunogenicity in tumor tissues should lead to more immunocyte infiltration as well as activation, thereby driving an antitumor immune response 33 .…”

Section: Resultsmentioning

confidence: 99%

B-Myb deficiency boosts bortezomib-induced immunogenic cell death in colorectal cancer

Hui,

Yu,

et al. 2024

Sci Rep

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“…Such immune cells are classified into two types based on their specific functions: active immune cells which offer antibody surveillance and block tumor growth, like CD8+ T cells & NK cells, and suppressing immune cells that aid in tumor expansion and progression, which include mainly Tregs, M2 macrophages, MDSCs, and Fig. 1 [34].…”

Section: Ovarian Cancer Immune Microenvironmentmentioning

confidence: 99%

Epithelial Ovarian Cancer: Microenvironment and Immunecheck Point Inhibitors

Kabala,

Bourhafour,

Chekrine

et al. 2023

EJMED

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With poor prognosis for patients with advanced disease, ovarian cancer continues to be the most lethal gynecologic malignancy. Despite optimal treatment, the disease frequently recurs and develops chemoresistance. The tumor immune microenvironment has been predicted to play a special role in tumor development and treatment, by modifying immunosuppressive and cytotoxic responses in close proximity to tumor cells via metabolic reprogramming. A better understanding of the tumor microenvironment’s critical roles allows researchers to develop new therapeutic strategies, such as immunotherapy, to combat epithelial ovarian cancer chemoresistance. Unfortunately, the results of many clinical trials examining immune checkpoint blockade (ICB) have shown very low levels of efficacy for single-agent immune checkpoint inhibitors, and research on combination treatments has not yet identified any combinations with robust activity in a large number of epithelial ovarian cancer patients. The present research will begin with a review of the main concept of immune response inside the ovarian cancer microenvironment. Then, we’ll try to figure out what role various immune checkpoint inhibitors have in the ovarian cancer microenvironment. Finally, we’ll look into several exciting treatment options, such as immune checkpoint inhibition and the body’s anti-ovarian cancer immunological response.

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“…Recent treatments combined with immune checkpoint blockade, PARP inhibition, chemotherapy, and antiangiogenic drugs have been widely encouraged in clinical trials for OC patients with advanced and metastatic stages. Still, the outcomes are inferior [ 5 ]. To date, accumulating evidence suggests that the high recurrence rate is thought to be due to remaining drug-resistant cells and cancer stem cells (CSC) [ 6 ].…”

Section: Introductionmentioning

confidence: 99%

A novel TCGA-validated programmed cell-death-related signature of ovarian cancer

Cai,

Lin,

Liu

et al. 2024

BMC Cancer

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Background Ovarian cancer (OC) is a gynecological malignancy tumor with high recurrence and mortality rates. Programmed cell death (PCD) is an essential regulator in cancer metabolism, whose functions are still unknown in OC. Therefore, it is vital to determine the prognostic value and therapy response of PCD-related genes in OC. Methods By mining The Cancer Genome Atlas (TCGA), Genotype-Tissue Expression (GTEx) and Genecards databases, we constructed a prognostic PCD-related genes model and performed Kaplan-Meier (K-M) analysis and Receiver Operating Characteristic (ROC) curve for its predictive ability. A nomogram was created via Cox regression. We validated our model in train and test sets. Quantitative real-time PCR (qRT-PCR) was applied to identify the expression of our model genes. Finally, we analyzed functional analysis, immune infiltration, genomic mutation, tumor mutational burden (TMB) and drug sensitivity of patients in low- and high-risk group based on median scores. Results A ten-PCD-related gene signature including protein phosphatase 1 regulatory subunit 15 A (PPP1R15A), 8-oxoguanine-DNA glycosylase (OGG1), HECT and RLD domain containing E3 ubiquitin protein ligase family member 1 (HERC1), Caspase-2.(CASP2), Caspase activity and apoptosis inhibitor 1(CAAP1), RB transcriptional corepressor 1(RB1), Z-DNA binding protein 1 (ZBP1), CD3-epsilon (CD3E), Clathrin heavy chain like 1(CLTCL1), and CCAAT/enhancer-binding protein beta (CEBPB) was constructed. Risk score performed well with good area under curve (AUC) (AUC3 − year =0.728, AUC5 − year = 0.730). The nomogram based on risk score has good performance in predicting the prognosis of OC patients (AUC1 − year =0.781, AUC3 − year =0.759, AUC5 − year = 0.670). Kyoto encyclopedia of genes and genomes (KEGG) analysis showed that the erythroblastic leukemia viral oncogene homolog (ERBB) signaling pathway and focal adhesion were enriched in the high-risk group. Meanwhile, patients with high-risk scores had worse OS. In addition, patients with low-risk scores had higher immune-infiltrating cells and enhanced expression of checkpoints, programmed cell death 1 ligand 1 (PD-L1), indoleamine 2,3-dioxygenase 1 (IDO-1) and lymphocyte activation gene-3 (LAG3), and were more sensitive to A.443,654, GDC.0449, paclitaxel, gefitinib and cisplatin. Finally, qRT-PCR confirmed RB1, CAAP1, ZBP1, CEBPB and CLTCL1 over-expressed, while PPP1R15A, OGG1, CASP2, CD3E and HERC1 under-expressed in OC cell lines. Conclusion Our model could precisely predict the prognosis, immune status and drug sensitivity of OC patients.

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Modulating the tumor immune microenvironment with nanoparticles: A sword for improving the efficiency of ovarian cancer immunotherapy

Cited by 7 publications

References 177 publications

B-Myb deficiency boosts bortezomib-induced immunogenic cell death in colorectal cancer

B-Myb deficiency boosts bortezomib-induced immunogenic cell death in colorectal cancer

Epithelial Ovarian Cancer: Microenvironment and Immunecheck Point Inhibitors

A novel TCGA-validated programmed cell-death-related signature of ovarian cancer

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