A miR-26a/E2F7 feedback loop contributes to tamoxifen resistance in ER-positive breast cancer

Liu, Jian; Li, Xiang; Wang, Meng; Xiao, Guodong; Yang, Guolong; Wang, Huangzhen; Li, Yanbo; Sun, Xin; Qin, Sida; Du, Ning; Ren, Hong; Pang, Yamei

doi:10.3892/ijo.2018.4492

Cited by 33 publications

(31 citation statements)

References 43 publications

(52 reference statements)

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“…OncoTargets and Therapy 2020:13 11910 cells. 33 Wang et al demonstrated that E2F7 abundance was enhanced in NSCLC tissues, and miR-935 restrained NSCLC progression through targeting and reducing E2F7 expression. 21 E2F7 was confirmed as a target of miR-33a-5p in NSCLC cells, and E2F7 silencing overturned circ_SATB2-mediated effects in Cela-treated NSCLC cells, suggested that circ_SATB2 functioned in Celastimulated NSCLC cells through enhancing E2F7 expression.…”

Section: Dovepressmentioning

confidence: 99%

<p>Circ_SATB2 Attenuates the Anti-Tumor Role of Celastrol in Non-Small-Cell Lung Carcinoma Through Targeting miR-33a-5p/E2F7 Axis</p>

Liu¹,

Wang²,

Tang³

et al. 2020

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Section: Dovepressmentioning

confidence: 99%

<p>Circ_SATB2 Attenuates the Anti-Tumor Role of Celastrol in Non-Small-Cell Lung Carcinoma Through Targeting miR-33a-5p/E2F7 Axis</p>

Liu¹,

Wang²,

Tang³

et al. 2020

OTT

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“…An MTT assay was used to measure the cell viability of MCF-7 and MDA-MB-231 lines. At 24 h post-transfection, cells were seeded in 96-well plates at a density of 4x10 3 cells/well and cultured for 24, 48 and 72 h. Then, the MTT assay was conducted as previously described (26).…”

Section: Reverse Transcription-quantitative Pcr (Rt-qpcr)mentioning

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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“…E2F7 has been found to be overexpressed in primary blasts isolated from patients with acute myeloid leukemia (AML), where it promoted cell cycle progression and inhibited the monocytic differentiation of AML cells ( 10 ). A previous study suggested that miR-26a and E2F7 may form a double-negative feedback loop, resulting in the downregulation of miR-26a and upregulation of E2F7 in estrogen receptor-positive breast cancer, where Both miR-26a knockdown and E2F7 overexpression conferred resistance to tamoxifen in MCF-7 cells ( 11 ). In addition, E2F7 has also been demonstrated to be overexpressed in cutaneous squamous cell carcinoma compared with that in normal epidermis, where suppression of E2F7 expression in a squamous cell carcinoma cell line resulted in increased UV-induced and doxorubicin-induced apoptosis ( 12 ).…”

Section: Introductionmentioning

confidence: 99%

E2F7, regulated by miR‑30c, inhibits apoptosis and promotes cell cycle of prostate cancer cells

Wáng

Pei

et al. 2020

Oncol Rep

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Prostate cancer (PCa) remains a leading cause of mortality among men in the United States and Western Europe. The molecular mechanism of PCa pathogenesis has not been fully elucidated. In the present study, the expression profile of E2F transcription factor 7 (E2F7) in PCa was examined using immunohistochemistry and reverse transcription-quantitative PCR, whilst cell cycle progression and apoptosis were determined using fluorescent cell activated sorting techniques. Cell viability was measured using Cell Counting Kit-8 in loss-and gain-of-function studies. Dual-luciferase reporter assay was used to verify if E2F7 was one of the potential targets of miR-30c. The staining score of E2F7 of PCa tissues was found to be notably higher compared with that of adjacent normal tissues. Suppression of E2F7 expression in PCa cell lines led to significantly reduced proliferation rates, increased proportion of cells in the G 1 phase of the cell cycle and higher apoptotic rates compared with those in negative control groups. Dual-luciferase reporter assay revealed E2F7 to be one of the binding targets of microRNA (miR)-30c. In addition, transfection of miR-30c mimics into PCa cells resulted in reduced cell viability, increased proportion of cells in the G 1 phase and higher apoptotic rates. By contrast, transfection with the miR-30c inhibitor led to lower apoptosis rates of PCa cells compared with negative control groups, whilst E2F7 siRNA co-transfection reversed stimulatory effects of miR-30c inhibitors on cell viability. In addition, the expression of cyclin-dependent kinase inhibitor p21 were found to be upregulated by transfection with either E2F7 siRNA or miR-30c mimics into PCa cells. In conclusion, the present study suggested that E2F7 may be positively associated with PCa cell proliferation by inhibiting p21, whereas E2F7 is in turn under regulation by miR-30c. These observations suggest the miR-30c/E2F7/p21 axis to be a viable therapeutic target for PCa.

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A miR-26a/E2F7 feedback loop contributes to tamoxifen resistance in ER-positive breast cancer

Cited by 33 publications

References 43 publications

<p>Circ_SATB2 Attenuates the Anti-Tumor Role of Celastrol in Non-Small-Cell Lung Carcinoma Through Targeting miR-33a-5p/E2F7 Axis</p>

<p>Circ_SATB2 Attenuates the Anti-Tumor Role of Celastrol in Non-Small-Cell Lung Carcinoma Through Targeting miR-33a-5p/E2F7 Axis</p>

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

E2F7, regulated by miR‑30c, inhibits apoptosis and promotes cell cycle of prostate cancer cells

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