GPER mediated estradiol reduces miR-148a to promote HLA-G expression in breast cancer

Tao, Sifeng; He, Haifei; Chen, Qiang; Yue, Wenjie

doi:10.1016/j.bbrc.2014.07.073

Cited by 45 publications

(40 citation statements)

References 35 publications

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“…Therefore, miRNAs have proven invaluable in the study of the mechanisms underlying BCL-2 expression in breast cancer. It has been reported that expression of miR-148a in breast cancer tissues is significantly reduced compared with matched normal tissues [14]. All of the above suggests that miR-148a may act as a tumor-suppressor gene in carcinogenesis.…”

Section: Discussionmentioning

confidence: 96%

“…Downregulation of miR-148a has been identified in both estrogen receptor-positive and triple-negative breast cancers [14]. Significant downregulation of miR-148a has also been reported in various cancers including glioblastoma [15], gastric cancer [16,17], pancreatic cancer [18], and hepatocellular cancer [19], in which miR-148a functions as a tumor-suppresser gene.…”

Section: Introductionmentioning

confidence: 98%

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MicroRNA-148a promotes apoptosis and suppresses growth of breast cancer cells by targeting B-cell lymphoma 2

Ren

Shi

et al. 2017

Anti-Cancer Drugs

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MicroRNAs (miRNAs) contribute toward tumorigenesis through the modulation of tumor-related genes. MiR-148a has been characterized as a tumor-suppressing miRNA and its downregulation has been reported in tumors of a variety of cancers. However, the functional role of miR-148a in breast cancer is not yet fully understood. Using both in-vitro and in-vivo models, we confirmed that miR-148a acts to inhibit the proliferation of breast cancer cells. Through the use of bioinformatic approaches in miRNA target prediction, we determined that B-cell lymphoma 2 (BCL-2) is a likely target of miR-148a. The overexpression and tumorigenic effects of BCL-2 have already been confirmed in cancerous tumors of the breast. A dual-luciferase assay was performed to confirm that miR-148a targets the 3'-untranslated region of BCL-2. In this study, we first characterized the downregulation of miR-148a in breast cancer tissues. We then found that restoring expression of miR-148a suppressed the expression of BCL-2 at the level of both mRNA and protein. Upregulation of miR-148a caused a subsequent reduction of proliferation and an increase in apoptosis. In conclusion, we have confirmed the role of miR-148a as a pivotal regulator in breast cancer through its targeting of BCL-2. This evidence strongly suggests that miR-148a could prove to be a novel therapeutic target in breast cancer.

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Section: Discussionmentioning

confidence: 96%

Section: Introductionmentioning

confidence: 98%

MicroRNA-148a promotes apoptosis and suppresses growth of breast cancer cells by targeting B-cell lymphoma 2

Ren

Shi

et al. 2017

Anti-Cancer Drugs

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“…A downregulation of miR-148a, which is closely involved in cancer cell proliferation, has been reported in both ER-positive breast cancer and TNBC. An experimental investigation (Tao et al 2014) has validated the hypothesis that E2 downregulates miR-148a through C protein-coupled oestrogen receptor-1 (GPER) and that E2 also affects the expression of HLA-G, which is an miR-148a target gene. Therefore, a new mechanism based on the ability of oestrogenic GPER signalling to trigger HLA-G expression through the inhibition of miR-148a, which supports immune evasion in breast cancer, has been elucidated.…”

Section: Relationships Between Tumour Growth and Immune Evasionmentioning

confidence: 91%

“…The expression of the enzyme arginase 1 (ARG 1) as a key mediator of immune suppression (Steggerda et al 2017) and the loss-of-function Janus-activated kinase (JAK) 1 mutations suggestive of immune suppression (Albacker et al 2017) have also been reported in multiple cancer types. Moreover, other recent studies have reported on immune evasion (Hix et al 2011, Khaled et al 2013, Markosyan et al 2013, Loumagne et al 2014, Tao et al 2014, Virtanen et al 2014, Olesch et al 2015,c, Zelenay et al 2015, Gameiro et al 2016, Heng et al 2016, Loi et al 2016.…”

Section: Mechanisms Of Immune Suppression or Immune Escapementioning

confidence: 96%

Tumour growth and immune evasion as targets for a new strategy in advanced cancer

Nicolini¹,

Rossi²,

Carpi³

2018

Endocrine-Related Cancer

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It has become clearer that advanced cancer, especially advanced breast cancer, is an entirely displayed pathological system that is much more complex than previously considered. However, the direct relationship between tumour growth and immune evasion can represent a general rule governing the pathological cancer system from the initial cancer cells to when the system is entirely displayed. Accordingly, a refined pathobiological model and a novel therapeutic strategy are proposed. The novel therapeutic strategy is based on therapeutically induced conditions (undetectable tumour burden and/or a prolonged tumour 'resting state'), which enable an efficacious immune response in advanced breast and other types of solid cancers.

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“…Specifically, several members of miR-148 family such as miR-148a, miR-148b, and miR-152 could downregulate HLA-G expression [65][66][67]. In breast cancer cells, it was observed that oncogenic estrogenic G-protein-coupled estrogen receptor-1 (GPER) signaling pathway decreased downstream miR-148a level, further contributing to cancer immune evasion [68]. Additionally, miR-133a was verified as a vital mediator in maintaining peripheral immune tolerance by targeting HLA-G [69].…”

Section: Hla-g-targeting Mirnasmentioning

confidence: 99%

The role of cancer-derived microRNAs in cancer immune escape

et al. 2020

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During malignant transformation, accumulated somatic mutations endow cancer cells with increased invasiveness and immunogenicity. Under selective pressure, these highly immunogenic cancer cells develop multiple strategies to evade immune attack. It has been well established that cancer cells could downregulate the expression of major histocompatibility complex, acquire alterations in interferon pathway, and upregulate the activities of immune checkpoint pathways. Besides, cancer cells secret numerous cytokines, exosomes, and microvesicles to regulate the functions and abundances of components in the tumor microenvironment including immune effector cells and professional antigen presentation cells. As the vital determinant of post-transcriptional regulation, microRNAs (miRNAs) not only participate in cancer initiation and progression but also regulate anti-cancer immune response. For instance, some miRNAs affect cancer immune surveillance and immune escape by interfering the expression of immune attack-associated molecules. A growing body of evidence indicated that cancer-derived immune modulatory miRNAs might be promising targets to counteract cancer immune escape. In this review, we summarized the role of some miRNAs in cancer immune escape and discussed their potential clinical application as treatment targets.

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GPER mediated estradiol reduces miR-148a to promote HLA-G expression in breast cancer

Cited by 45 publications

References 35 publications

MicroRNA-148a promotes apoptosis and suppresses growth of breast cancer cells by targeting B-cell lymphoma 2

MicroRNA-148a promotes apoptosis and suppresses growth of breast cancer cells by targeting B-cell lymphoma 2

Tumour growth and immune evasion as targets for a new strategy in advanced cancer

The role of cancer-derived microRNAs in cancer immune escape

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