miR‐511 inhibits proliferation and metastasis of breast cancer cells by targeting FGF4

Zhang, Chao; Yang, Ting; Jiang, Hongchuan

doi:10.1002/jgm.3168

Cited by 19 publications

(20 citation statements)

References 30 publications

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“…The expression of MiR-32 is markedly lower in ovarian cancer tissues than that in adjacent normal tissues; miR-32 also directly targets the 3′-UTR of BTLA ( 123 ). BTLA is a new member of the CD28 family ( 34 ).…”

Section: The Impact Of Mirna Targeting Btla On Cancermentioning

confidence: 99%

“…Previous research showed that miR-32 can suppress the malignant behavior of HeLa cells ( 124 ). Moreover, the high expression level of BTLA could significantly play an anticancer role in miR-32, while the overexpression of miR-32 could greatly inhibit the mRNA and protein expressions of BTLA ( 123 ). A negative feedback loop was formed between miR-32 and BTLA, regulating the malignant behavior of ovarian cancer cells ( 123 ).…”

Section: The Impact Of Mirna Targeting Btla On Cancermentioning

confidence: 99%

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The Role of NcRNAs to Regulate Immune Checkpoints in Cancer

Jiang

Zhao

et al. 2022

Front. Immunol.

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At present, the incidence of cancer is becoming more and more common, but its treatment has always been a problem. Although a small number of cancers can be treated, the recurrence rates are generally high and cannot be completely cured. At present, conventional cancer therapies mainly include chemotherapy and radiotherapy, which are the first-line therapies for most cancer patients, but there are palliatives. Approaches to cancer treatment are not as fast as cancer development. The current cancer treatments have not been effective in stopping the development of cancer, and cancer treatment needs to be imported into new strategies. Non-coding RNAs (ncRNAs) is a hot research topic at present. NcRNAs, which include microRNAs (miRNAs), circular RNAs (circRNAs), and long non-coding RNAs (lncRNAs), participate in all aspects of cancer biology. They are involved in the progression of tumors into a new form, including B-cell lymphoma, glioma, or the parenchymal tumors such as gastric cancer and colon cancer, among others. NcRNAs target various immune checkpoints to affect tumor proliferation, differentiation, and development. This might represent a new strategy for cancer treatment.

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Section: The Impact Of Mirna Targeting Btla On Cancermentioning

confidence: 99%

Section: The Impact Of Mirna Targeting Btla On Cancermentioning

confidence: 99%

The Role of NcRNAs to Regulate Immune Checkpoints in Cancer

Jiang

Zhao

et al. 2022

Front. Immunol.

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“…MiR-NAs have been recognized as the main regulators of cancer development as well. For instance, miR-511 was described to suppress breast cancer cell proliferation and invasion through targeting FGF4 [21]. In this study, we found miR-3196 could bind with MAFG-AS1.…”

Section: Discussionmentioning

confidence: 51%

MAFG-AS1 aggravates the progression of pancreatic cancer by sponging miR-3196 to boost NFIX

Feng

Weng

et al. 2020

Cancer Cell Int

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Background A host of researches have demonstrated the regulation of long non-coding RNAs (lncRNAs) in the progression of pancreatic cancers (PC). In this study, our main task was to analyze the function of MAF bZIP transcription factor G antisense RNA 1 (MAFG-AS1) in PC. Methods RT-qPCR measured gene expression. Functional experiments, including EdU assay, flow cytometry analysis, TUNEL assay and transwell assay, assessed the biological changes of PC cells. RNA pull down assay, luciferase reporter assay and RIP assay verified the interaction between RNAs. Results MAFG-AS1 was lowly expressed in normal pancreatic samples but up-regulated in PC tissues and cell lines. Besides, MAFG-AS1 silence suppressed cell proliferation and migration whereas promoted cell apoptosis in PC. Mechanism assays verified that miR-3196 could bind with MAFG-AS1. Moreover, miR-3196 was discovered to be lowly expressed in PC cell lines, and its overexpression inhibited PC cell growth and migration. Importantly, nuclear factor I X (NFIX), overexpressed in PC cell lines, was validated to be positively modulated by MAFG-AS1 through absorbing miR-3196. Moreover, overexpression of NFIX could countervail the restraining effects of MAFG-AS1 knockdown on the growth and migration of PC cells. Conclusion MAFG-AS1 had an oncogenic function in the progression of PC via regulating miR-3196/NFIX pathway, and decreasing MAFG-AS1 expression could attenuate PC progression.

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“…Another explanation might be that as many different miRs are upregulated in CLL cells, they can also be responsible for abnormal BTLA expression and in consequence could partially mask the effect of miR-155-5p inhibition. Until now only miR-32 has been described to regulate BTLA expression [ 48 ], thus, we cannot exclude the influence of other miRs on BTLA expression in CLL cells. Silencing of miR-155-5p did not have significant influence on BTLA expression in the case of HC B cells.…”

Section: Discussionmentioning

confidence: 99%

BTLA Expression in CLL: Epigenetic Regulation and Impact on CLL B Cell Proliferation and Ability to IL-4 Production

Karabon

Andrzejczak

Ciszak

et al. 2021

Cells

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In our previous study, while chronic lymphocytic leukemia (CLL) cases showed higher levels of B and T lymphocyte attenuator (BTLA) mRNA compared to controls, lower BTLA protein expression was observed in cases compared to controls. Hence we hypothesize that micro RNA (miR) 155-5p regulates BTLA expression in CLL. In line with earlier data, expression of BTLA mRNA and miR-155-5p is elevated in CLL (p = 0.034 and p = 0.0006, respectively) as well as in MEC-1 cell line (p = 0.009 and 0.016, respectively). Inhibition of miR-155-5p partially restored BTLA protein expression in CLL patients (p = 0.01) and in MEC-1 cell lines (p = 0.058). Additionally, we aimed to evaluate the significance of BTLA deficiency in CLL cells on proliferation and IL-4 production of B cells. We found that secretion of IL-4 is not dependent on BTLA expression, since fractions of BTLA positive and BTLA negative B cells expressing intracellular IL-4 were similar in CLL patients and controls. We demonstrated that in controls the fraction of proliferating cells is lower in BTLA positive than in BTLA negative B cells (p = 0.059), which was not observed in CLL. However, the frequency of BTLA positive Ki67+ B cells in CLL was higher compared to corresponding cells from controls (p = 0.055) while there were no differences between the examined groups regarding frequency of BTLA negative Ki67+ B cells. Our studies suggest that miR-155-5p is involved in BTLA deficiency, affecting proliferation of CLL B cells, which may be one of the mechanisms responsible for CLL pathogenesis.

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miR‐511 inhibits proliferation and metastasis of breast cancer cells by targeting FGF4

Cited by 19 publications

References 30 publications

The Role of NcRNAs to Regulate Immune Checkpoints in Cancer

The Role of NcRNAs to Regulate Immune Checkpoints in Cancer

MAFG-AS1 aggravates the progression of pancreatic cancer by sponging miR-3196 to boost NFIX

BTLA Expression in CLL: Epigenetic Regulation and Impact on CLL B Cell Proliferation and Ability to IL-4 Production

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