MicroRNA-124 enhances response to radiotherapy in human epidermal growth factor receptor 2-positive breast cancer cells by targeting signal transducer and activator of transcription 3

Fu, Ying; Xiong, Jianping

doi:10.3325/cmj.2016.57.457

Cited by 18 publications

(13 citation statements)

References 26 publications

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“…Overexpression of miR-124 reduced the activity of STAT3 signaling pathway and enhanced apoptosis upon irradiation in NSCLC and in HER2-positive breast cancer [37,38]. In line with these findings, low miR-124 and high STAT3 levels were associated with a poor response to radiotherapy in HER2-positive breast cancer patients [38]. Ectopic expression of miR-320a enhanced IR-induced apoptosis and radiosensitivity of NSCLC cells both in vitro and in vivo [60].…”

Section: Mirnassupporting

confidence: 54%

“…STAT3, one of the main players in the JAK/STAT pathway, is a direct target of miR-124, miR-320a and miR-634 [37,60,68]. Overexpression of miR-124 reduced the activity of STAT3 signaling pathway and enhanced apoptosis upon irradiation in NSCLC and in HER2-positive breast cancer [37,38]. In line with these findings, low miR-124 and high STAT3 levels were associated with a poor response to radiotherapy in HER2-positive breast cancer patients [38].…”

Section: Mirnasmentioning

confidence: 99%

“…We also present an overview of ncRNAs that alter radiosensitivity of cancer cells (Tables 1 and 2) and discuss the utilization of ncRNAs to improve the outcome of radiotherapy. [16,17] miR- 16 Cyclin D1 Cell cycle Prostate cancer [18] miR-18a ATM DSB repair Breast cancer, lung cancer * [19,20] HIF-1α -Lung cancer * [20] miR-22 SIRT1 Apoptosis Breast cancer [21] miR-23b ATG12 Autophagy Pancreatic cancer * [22] miR-24 H2AX DSB repair Leukemia [23] miR-26a ATM DSB repair Glioma [24] miR-26b DRAM1 Autophagy Breast cancer [25] miR-30a TP53INP1 Autophagy Prostate cancer [26] miR-33a HIF-1α Glycolysis Melanoma * [27] miR-34a LyGDI Apoptosis NSCLC [28] RAD51 DSB repair Lung cancer * [29] miR-99a mTOR Apoptosis NSCLC * [30] miR-100 ATM -Glioma [31] miR-101 DNA-PKcs -Glioma * [32] ATM -Glioma * [32] STMN1 Autophagy NPC [33] miR-107 RAD51 DSB repair Ovarian cancer [34] miR-124 CDK4 Apoptosis Glioma, ESCC [35,36] STAT3 Apoptosis NSCLC *, breast cancer [37,38] PIM 1 -Prostate cancer [39] miR-125a p21 -Cervical cancer [40] miR-125b c-Jun Apoptosis Breast cancer [41] miR-133a EGFR Apoptosis ESCC [42] miR-133b PKM2 Glycolysis NSCLC [43] miR-136 E2F1 Apoptosis Cervical cancer [44] [45] miR-144 PIM 1 -Prostate cancer [39] miR-150 AKT Apoptosis NK/T cell lymphoma * [46] miR-153 Bcl-2 Apoptosis Glioma * [47] miR-155 RAD51 DSB repair Triple negative breast cancer *…”

Section: Introductionmentioning

confidence: 99%

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Non-Coding RNAs in Cancer Radiosensitivity: MicroRNAs and lncRNAs as Regulators of Radiation-Induced Signaling Pathways

Podralska

Ciesielska

Kluiver

et al. 2020

Cancers

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Radiotherapy is a cancer treatment that applies high doses of ionizing radiation to induce cell death, mainly by triggering DNA double-strand breaks. The outcome of radiotherapy greatly depends on radiosensitivity of cancer cells, which is determined by multiple proteins and cellular processes. In this review, we summarize current knowledge on the role of microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), in determining the response to radiation. Non-coding RNAs modulate ionizing radiation response by targeting key signaling pathways, including DNA damage repair, apoptosis, glycolysis, cell cycle arrest, and autophagy. Additionally, we indicate miRNAs and lncRNAs that upon overexpression or inhibition alter cellular radiosensitivity. Current data indicate the potential of using specific non-coding RNAs as modulators of cellular radiosensitivity to improve outcome of radiotherapy.

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Section: Mirnassupporting

confidence: 54%

Section: Mirnasmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Non-Coding RNAs in Cancer Radiosensitivity: MicroRNAs and lncRNAs as Regulators of Radiation-Induced Signaling Pathways

Podralska

Ciesielska

Kluiver

et al. 2020

Cancers

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show abstract

“…Notably, miR-124 overexpression inhibits cell growth, migration, invasion and chemoresistance in breast cancer (19)(20)(21). Furthermore, miR-124 overexpression enhances the sensitivity of HER2-positive breast cancer cells to irradiation by directly targeting STAT3 (22). However, the association between NEAT1, miR-124 and STAT3 in breast cancer is not fully understood.…”

Section: Introductionmentioning

confidence: 99%

NEAT1/miR‑124/STAT3 feedback loop promotes breast cancer progression

Pang

et al. 2019

Int J Oncol

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The long non-coding RNA nuclear enriched abundant transcript 1 (NEAT1) has important roles in the regulation of multiple cell functions, such as proliferation, apoptosis and migration. However, the mechanism by which NEAT1 regulates breast cancer progression is not well elucidated. In the present study, NEAT1 and microRNA-124 (miR-124) levels were detected by reverse transcription-quantitative PCR in breast cancer tissues and cell lines. STAT3 protein levels were detected by western blot analysis. Cell proliferation and cell cycle distribution were determined using MTT and colony formation assays, and flow cytometry, respectively. The results demonstrated that NEAT1 and STAT3 expression levels were increased in breast cancer tissues compared with normal breast tissues, whereas miR-124 expression was significantly decreased. Functional analyses revealed that NEAT1 promoted cell proliferation and cell cycle progression in breast cancer cells. Additionally, NEAT1 and STAT3 expression levels were negatively correlated with miR-124 levels in breast cancer tissues. A direct interaction between miR-124, and NEAT1 and STAT3, was predicted by bioinformatics analysis and confirmed using a luciferase activity assay. NEAT1 overexpression markedly increased STAT3 protein expression levels, and this effect was reversed by miR-124 overexpression in breast cancer cells. Furthermore, miR-124 overexpression partially attenuated the effects of NEAT1 on breast cancer cell proliferation and cell cycle progression. The inhibitory effects of miR-124 overexpression on the proliferation rate and cell cycle progression were abolished by STAT3 overexpression. In turn, STAT3 silencing inhibited NEAT1 transcription in breast cancer cells. In summary, the present findings revealed that NEAT1 and STAT3 formed a feedback loop via sponging miR-124 to promote breast cancer progression.

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“…In the study by Sirkisoon, S. R et al, STAT3 undergoes protein-protein interactions with glioma oncogene homolog 1 (GLI1) and (truncated GLI1) tGLI1, which promote gene activation and a stem-like phenotype of breast cancer [14]. Furthermore, the target relationship between miR-124 and STAT3 has been revealed in human epidermal growth factor receptor 2 (HER2)-positive breast cancer cells [15]. How STAT3 interacts with miR-124 in BCSCs is still unclear.…”

Section: Introductionmentioning

confidence: 99%

MiR-124 reversed the doxorubicin resistance of breast cancer stem cells through STAT3/HIF-1 signaling pathways

et al. 2019

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Various drug treatments including doxorubicin (DOX) have been proved efficient in the suppression of breast cancer. Nonetheless, drug resistance became an obstacle in the therapeutic process. According to recent literatures, breast cancer stem cells (BCSCs) were considered contributing to drug resistance, besides, microRNAs (miRNAs) could regulate proteins associated with drug resistance in human breast cancer. To further understand the inner mechanism of drug resistance in breast cancer and look for remedy methods, we referred to bioinformatic analysis and predicted that signal transducer and activator of transcription 3 (STAT3) and miR-124 was overexpressed in MCF7-R cells (MCF7 cells resistant to DOX) compared with MCF cells. Expression levels of RNA and protein were separately determined by qRT-PCR and western blot. Dual luciferase assay was performed to verify the targeting relationship between STAT3 and miR-124. Optical density (OD) values and apoptotic rates of cells were respectively determined via MTT assays and flow cytometric analysis. Cell invasion was detected to verify drug resistance. Results of above assays indicated that STAT3 was highly expressed in MCF7-R cells than in MCF7 cell lines and affected doxorubicin resistance of BCSCs, and miR-124 reversed the doxorubicin resistance of breast cancer stem cells through targeting STAT3 to control the HIF-1 signaling pathway. To conclude, this research may be valuable for the treatment of breast cancer as the restoration of miR-124 and inhibition of STAT3 could be applied to therapeutic strategy and help overcome drug resistance.

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MicroRNA-124 enhances response to radiotherapy in human epidermal growth factor receptor 2-positive breast cancer cells by targeting signal transducer and activator of transcription 3

Cited by 18 publications

References 26 publications

Non-Coding RNAs in Cancer Radiosensitivity: MicroRNAs and lncRNAs as Regulators of Radiation-Induced Signaling Pathways

Non-Coding RNAs in Cancer Radiosensitivity: MicroRNAs and lncRNAs as Regulators of Radiation-Induced Signaling Pathways

NEAT1/miR‑124/STAT3 feedback loop promotes breast cancer progression

MiR-124 reversed the doxorubicin resistance of breast cancer stem cells through STAT3/HIF-1 signaling pathways

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