Noncoding RNAs link metabolic reprogramming to immune microenvironment in cancers

Zhang, Yiyin; Mao, Qijiang; Xia, Qinglin; Cheng, Jiaxi; Huang, Zhenzhen; Li, Yirun; Chen, Peng; Yang, Jing; Fan, Xiaohui; Liang, Yuelong; Lin, Hui

doi:10.1186/s13045-021-01179-y

Cited by 53 publications

(27 citation statements)

References 321 publications

(295 reference statements)

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“…More and more evidence confirmed that noncoding RNA (ncRNA) plays an important role in mediating breast cancer genesis and progression [ 6 ]. MicroRNAs (miRNA) are small noncoding RNAs with nucleotides of 19-25 in length that can regulate posttranscription gene expression.…”

Section: Introductionmentioning

confidence: 99%

[Retracted] The Function of circRNA‐0047604 in Regulating the Tumor Suppressor Gene DACH1 in Breast Cancer

Zhao

Zhou

et al. 2022

BioMed Research International

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Breast cancer is the most common cancer among females. Dachshund Homolog 1 (DACH1) gene is regarded as an important tumor suppressor gene in breast cancer which plays an important regulatory role in the development disease progression, particularly in carcinomas. Circular RNAs (circRNAs) and microRNA (miRNA), regarded as a novel group of noncoding RNAs, are always involved in regulating gene expression. In this work, hsa_circ_0047604 expressed lower in breast cancer tissue and played the role of sponge of miR-548o. By this way, hsa_circ_0047604 could upregulate DACH1 to inhibit breast cancer. In conclusion, this study revealed that hsa_circ_0047604 acted as a tumor suppressor and regulated breast cancer progression via hsa_circ_0047604–miR-548o–DACH1 axis, which might provide a therapeutic method for breast cancer.

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Section: Introductionmentioning

confidence: 99%

[Retracted] The Function of circRNA‐0047604 in Regulating the Tumor Suppressor Gene DACH1 in Breast Cancer

Zhao

Zhou

et al. 2022

BioMed Research International

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“…Based on this concept and these research results, TVEC has been approved by the US FDA for clinical use in patients with advanced malignant melanoma. While intratumoral administration of immunostimulatory agents and noncoding RNAs in solid tumors is a plausible method [ 140 ] and may remodel tumor metabolism and the immune microenvironment [ 141 , 142 ], due to the pathogenesis of AML and MDS, intratumoral vaccination to locally activate tumor-infiltrating DCs may not be widely applicable except in the cases with chloroma as the only presentation.…”

Section: Methods For Vaccine Deliverymentioning

confidence: 99%

Research progress on dendritic cell vaccines in cancer immunotherapy

Sun

Cao

et al. 2022

Exp Hematol Oncol

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Dendritic cell (DC) vaccines induce specific immune responses that can selectively eliminate target cells. In recent years, many studies have been conducted to explore DC vaccination in the treatment of hematological malignancies, including acute myeloid leukemia and myelodysplastic syndromes, as well as other nonleukemia malignancies. There are at least two different strategies that use DCs to promote antitumor immunity: in situ vaccination and canonical vaccination. Monocyte-derived DCs (mo-DCs) and leukemia-derived DCs (DCleu) are the main types of DCs used in vaccines for AML and MDS thus far. Different cancer-related molecules such as peptides, recombinant proteins, apoptotic leukemic cells, whole tumor cells or lysates and DCs/DCleu containing a vaster antigenic repertoire with RNA electroporation, have been used as antigen sources to load DCs. To enhance DC vaccine efficacy, new strategies, such as combination with conventional chemotherapy, monospecific/bispecific antibodies and immune checkpoint-targeting therapies, have been explored. After a decade of trials and tribulations, much progress has been made and much promise has emerged in the field. In this review we summarize the recent advances in DC vaccine immunotherapy for AML/MDS as well as other nonleukemia malignancies.

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“…Cancer cells and TAMs establish a mutual metabolic communication, with cancer cells promoting the M2-like phenotype through the secretion of lactate, and TAMs increasing glucose availability for tumor cells [84]. Non-coding RNAs are crucial mediators of this interplay [85,86].…”

Section: Non-coding Rnas In the Regulation Of Bc Cells And Tam Metabo...mentioning

confidence: 99%

Non-Coding RNAs in the Crosstalk between Breast Cancer Cells and Tumor-Associated Macrophages

Benedetti

Turco

Fontemaggi

et al. 2022

ncRNA

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Non-coding RNAs (ncRNAs) play a pivotal role in regulating the tumor microenvironment (TME) by controlling gene expression at multiple levels. In tumors, ncRNAs can mediate the crosstalk between cancer cells and other cells in the TME, such as immune cells, stromal cells, and endothelial cells, influencing tumor development and progression. Tumor-associated macrophages (TAMs) are among the most abundant inflammatory cells infiltrating solid cancers that promote tumorigenesis, and their infiltration correlates with a poor prognosis in many tumors. Cancer cells produce different ncRNAs that orchestrate TAM recruitment and polarization toward a tumor-promoting phenotype. Tumor-reprogrammed macrophages shape the TME by promoting angiogenesis and tissue remodeling, and suppressing the anti-tumor activity of adaptive immune cells. TAMs can also produce ncRNA molecules that boost cancer cell proliferation and direct their phenotype and metabolic changes facilitating cancer progression and metastasis. This review will focus on the crosstalk between cancer cells and TAMs mediated by microRNAs and long non-coding RNAs during breast cancer (BC) initiation and progression.

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Noncoding RNAs link metabolic reprogramming to immune microenvironment in cancers

Cited by 53 publications

References 321 publications

[Retracted] The Function of circRNA‐0047604 in Regulating the Tumor Suppressor Gene DACH1 in Breast Cancer

[Retracted] The Function of circRNA‐0047604 in Regulating the Tumor Suppressor Gene DACH1 in Breast Cancer

Research progress on dendritic cell vaccines in cancer immunotherapy

Non-Coding RNAs in the Crosstalk between Breast Cancer Cells and Tumor-Associated Macrophages

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