Suppressive effect of exogenous miR‐16 and miR‐34a on tumorigenesis of breast cancer cells

Haghi, Mehdi; Taha, Masoumeh Fakhr; Javeri, Arash

doi:10.1002/jcb.28608

Cited by 33 publications

(21 citation statements)

References 49 publications

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“…Upregulation of β‐catenin expression in both MDA‐miR‐302/367 and SK‐miR‐302/367 cells by miR‐16 inhibitor indicates an important role for miR‐16 in regulation of β‐catenin in the BC cells. Suppression of vimentin and β‐catenin proteins by miR‐16 has previously been reported in oral squamous cell carcinoma, ovarian cancer cells, chordoma cells, and breast cancer cells by our group . MiR‐16 has been shown as an important suppressor of Wnt/β‐catenin signaling pathway, which targets WNT3A and Frizzled receptor gene, FZD6 , as two important factors of β‐catenin signaling cascade.…”

Section: Discussionsupporting

confidence: 54%

“…In this study, we showed that transfection of BC cells with miR‐302/367 cluster and miR‐16 mimic leads to downregulation of SMAD2 and upregulation of TGFBR2 . We previously showed that either miR‐16 or miR‐302/367 cluster can downregulate SMAD3 expression in MDA‐MB‐231 and SK‐BR‐3 cells . Bioinformatic analyses using several databases including TargetScan, miRTarBase, and TarBase and previous reports have shown that some TGF‐β signaling factors such as TGFBR3 , TGFB1 , SMAD2 , SMAD3 , SMURF1 , ACVR2a , and TGFBR2 are miR‐16 targets .…”

Section: Discussionmentioning

confidence: 99%

“…Suppression of vimentin and β-catenin proteins by miR-16 has previously been reported in oral squamous cell carcinoma, 40 ovarian cancer cells, 41 chordoma cells, 42 and breast cancer cells by our group. 21 MiR-16 has been shown as an important suppressor of Wnt/β-catenin signaling pathway, 41 which targets WNT3A and Frizzled receptor gene, FZD6, as two important factors of β-catenin signaling cascade. Upregulation of β-catenin protein in the breast cancer cells by miR-16 inhibitor indicates a significant role for miR-16 in regulation of β-catenin expression and Wnt/β-catenin signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

“…Several studies have shown the inhibitory effect of miR‐16 on tumorigenicity of different cancer cells through suppression of proliferation, invasion, migration, angiogenesis, and induction of apoptosis . Also, miR‐16 suppresses the expression of TGF‐β and some epithelial–mesenchymal transition (EMT)‐related genes .…”

Section: Introductionmentioning

confidence: 99%

“…17 Several studies have shown the inhibitory effect of miR-16 on tumorigenicity of different cancer cells through suppression of proliferation, invasion, migration, angiogenesis, and induction of apoptosis. [18][19][20][21] Also, miR-16 suppresses the expression of TGF-β and some epithelial-mesenchymal transition (EMT)-related genes. 22 The aim of this study was to assess the impact of exogenous mature miR-16 on both reprogramming and tumorigenicity of human breast cancer cells, which are under the influence of miR-302/367 overexpression, and whether miR-16 can serve as an effective adjuvant for tumor-suppressive function of miR-302/367.…”

Section: Introductionmentioning

confidence: 99%

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miR‐16 enhances miR‐302/367‐induced reprogramming and tumor suppression in breast cancer cells

2020

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Overexpression of either miR‐302 or miR‐302/367 cluster induces reprogramming of cancer cells and exerts tumor‐suppressive effects by induction of mesenchymal‐to‐epithelial transition, apoptosis and a less proliferative capacity. Several reports have described miR‐16 as a tumor suppressor microRNA (miRNA). Here, we studied the impact of exogenous induction of miR‐16 in MDA‐MB‐231 and SK‐BR‐3 breast cancer cells following overexpression of miR‐302/367 cluster and investigated whether transfection of these cells by a mature miR‐16 mimic could affect the reprogramming state of the cells and their tumorigenicity. miR‐16 enhanced the expression levels of OCT4A, SOX2, and NANOG, generally known as transcription or pluripotency factors, and suppressed proliferation and invasiveness of these cells. Meanwhile, inhibition of miR‐16 counteracted both the reprogramming effect and the antitumor function of miR‐302/367 in the breast cancer cells. Current results indicate that miR‐16 can work as an adjuvant to improve both cancer cell reprogramming and tumor‐suppressive function of miR‐302/367 cluster in MDA‐MB‐231 and SK‐BR‐3 cells, while its inhibition counteracts all of these effects. Combined application of miRNAs that share some common targets in cancer cell signaling pathways may provide new approaches for repression of multiple hallmarks of cancer.

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Section: Discussionsupporting

confidence: 54%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

miR‐16 enhances miR‐302/367‐induced reprogramming and tumor suppression in breast cancer cells

2020

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A novel role for aspirin in enhancing the reprogramming function of miR‐302/367 cluster and breast tumor suppression

Rezania

Eghtedari

Taha

et al. 2022

J of Cellular Biochemistry

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Recent studies have provided evidence for tumor suppressive function of the embryonic stem cell‐specific miR‐302/367 cluster through induction of a reprogramming process. Aspirin has been found to induce reprogramming factors of mesenchymal‐to‐epithelial transition in breast cancer cells. Therefore, we aimed to investigate whether overexpression of miR‐302/367 cluster and aspirin treatment cooperate in the induction of reprogramming and tumor suppression in breast cancer cells. MDA‐MB‐231 and SK‐BR‐3 human breast cancer cell lines were transfected with a miR‐302/367 expressing vector and treated with aspirin. The cells were evaluated for indices of apoptosis, proliferation, migration, and invasion. In both cell lines, treatment of miR‐302/367‐transfected cells with aspirin upregulated expression of some main pluripotency factors such as OCT4, SOX2, NANOG, and KLF4, and downregulated expression of some invasion and angiogenesis markers at gene and protein levels. Aspirin increased the apoptotic rate in both cell lines transfected with miR‐302/367. Both miR‐302/367 and aspirin upregulated the expression of FOXD3 protein which is a known inducer of OCT4 and NANOG. Our results demonstrate that aspirin can enhance miR‐302/367‐induced reprogramming of breast cancer cells possibly through upregulation of FOXD3 expression. This can further augment the reversal of epithelial–mesenchymal transition and inhibits migration, invasion, and angiogenic signaling in breast cancer cells reprogrammed by miR‐302/367. Therefore, aspirin may serve as a useful adjuvant for reprogramming of cancer cells.

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Exploring the time-dependent regulatory potential of microRNAs in breast cancer cells treated with proteasome inhibitors

Katsaraki,

Kontos,

Ardavanis-Loukeris

et al. 2023

Clin Transl Oncol

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Purpose Breast cancer (BrCa) is a predominant type of cancer with a disparate molecular nature. MicroRNAs (miRNAs) have emerged as promising key players in the regulation of pathological processes in BrCa. Proteasome inhibitors (PIs) emerged as promising anticancer agents for several human malignancies, including BrCa, inhibiting the function of the proteasome. Aiming to shed light on the miRNA regulatory effect in BrCa after treatment with PIs, we used two PIs, namely bortezomib and carfilzomib. Materials and methods Four BrCa cell lines of distinct molecular subtypes were treated with these PIs. Cell viability and IC50 concentrations were determined. Total RNA was extracted, polyadenylated, and reversely transcribed. Next, the levels of specific miRNAs with a significant role in BrCa were determined using relative quantification, and their regulatory effect was assessed. Results High heterogeneity was discovered in the levels of miRNAs in the four cell lines, after treatment. The miRNA levels fluctuate with distinct patterns, in 24, 48, or 72 hours. Interestingly, miR-1-3p, miR-421-3p, and miR-765-3p appear as key molecules, as they were found deregulated, in almost all combinations of cell lines and PIs. In the SK-BR-3 cell line, the majority of the miRNAs were significantly downregulated in treated compared to untreated cells, with miR-21-5p being the only one upregulated. Finally, various significant biological processes, molecular functions, and pathways were predicted to be affected. Conclusions The diversity of pathways predicted to be affected by the diversity in miRNA expression after treatment with PIs paves the way for the recognition of new regulatory axes in BrCa.

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Suppressive effect of exogenous miR‐16 and miR‐34a on tumorigenesis of breast cancer cells

Cited by 33 publications

References 49 publications

miR‐16 enhances miR‐302/367‐induced reprogramming and tumor suppression in breast cancer cells

miR‐16 enhances miR‐302/367‐induced reprogramming and tumor suppression in breast cancer cells

A novel role for aspirin in enhancing the reprogramming function of miR‐302/367 cluster and breast tumor suppression

Exploring the time-dependent regulatory potential of microRNAs in breast cancer cells treated with proteasome inhibitors

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