miR-27b-3p inhibits proliferation and potentially reverses multi-chemoresistance by targeting CBLB/GRB2 in breast cancer cells

Chen, Danni; Si, Wengong; Shen, Jingnan; Du, Chengyong; Lou, Weiyang; Bao, Chang; Zheng, Huilin; Pan, Jie; Zhong, Guansheng; Xu, Liang; Fu, Peifen; Fan, Weimin

doi:10.1038/s41419-017-0211-4

Cited by 114 publications

(98 citation statements)

References 43 publications

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“…This work followed the expression analyses of miRNA profiles in our previous studies, which showed that downregulated miR‐27b was confirmed in OLP tissues when compared with tissues from healthy subjects. In a similar manner, miR‐27b was previously reported as a tumor suppressor, which was decreased or depleted in colorectal cancer, gastric cancer, breast cancer, and in oral squamous cell carcinoma . Moreover, Aghbariet et al reported decreased expressions of miR‐27b in tissues of OLP patients when compared with control samples, which was consistent with our results.…”

Section: Discussionsupporting

confidence: 92%

“…For example, Matsuyama et al reported a tumor suppressive role for miR‐27b in human colon cancer cells. Chen et al showed that downregulation of miR‐27b was correlated with cell proliferation by inactivating the phosphatidylinositol‐3‐kinase/protein kinase B signaling pathways in breast cancers. In addition, Liu et al reported that decreased miR‐27b promoted oral squamous cell carcinoma cell proliferation by targeting Frizzled‐7 and contributing to tumorigenesis.…”

Section: Introductionmentioning

confidence: 99%

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Downregulated miR‐27b promotes keratinocyte proliferation by targeting PLK2 in oral lichen planus

Chen

Chang

et al. 2019

J Oral Pathology Medicine

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Background: was recently found to be significantly downregulated in oral lichen planus (OLP). However, evidence of the function of miR-27b in OLP remains limited. Methods:Initially, miR-27b expression in OLP was verified using the quantitative real-time polymerase chain reaction (qRT-PCR). Functionally, gain-/loss-of-function studies were then conducted using miR-27b mimics/inhibitor to investigate cell growth in human oral keratinocytes (HOKs). Mechanistically, subsequent miRNA target analyses including a starBase database analysis and a luciferase reporter assay were performed to predict and validate the direct target, respectively. In addition, overexpression/knockdown assays of target(s) of miR-27b were performed to investigate its functional significance and qRT-PCR and western blotting were used to evaluate the target(s) of miR-27b mRNA and protein levels, respectively. Results:MicroRNA-27b was significantly downregulated in OLP tissues when compared with healthy control tissues. Bioinformatics predicted that Polo Like Kinase 2 (PLK2) might be a potential target of miR-27b, while the luciferase reporter assay results showed the direct inhibition of the plk2-3′untranslated region by miR-27b.Moreover, functional analysis indicated that downregulated miR-27b caused an increase in cell growth in HOKs, and correspondingly, overexpression of PLK2 promoted HOK proliferation.Conclusions: There were aberrant expressions of miR-27b and PLK2 in OLP tissues.Decreased miR-27b may have induced cell proliferation by increasing the levels of PLK2 in HOKs, which provides a new perspective into the potential mechanisms underlying OLP development. K E Y W O R D Skeratinocytes, miR-27b, oral lichen planus, PLK2, Proliferation

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Downregulated miR‐27b promotes keratinocyte proliferation by targeting PLK2 in oral lichen planus

Chen

Chang

et al. 2019

J Oral Pathology Medicine

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“…Our data are therefore consistent with a role of miR‐27a as tumour suppressor and that its downregulation leads to an upregulation of the pro‐oncogenic CBLB and CCNG1. Interestingly, a report indicated that miR‐27b, another member of the miR‐27 family, directly targets CBLB [54], though it is not clear whether miR‐27a and miR‐27b can interact with the same mRNA targets or are cell type‐specific.…”

Section: Discussionmentioning

confidence: 99%

Deregulation of miR‐27a may contribute to canine fibroblast activation after coculture with a mast cell tumour cell line

et al. 2020

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The tumour microenvironment comprises a diverse range of cells, including fibroblasts, immune cells and endothelial cells, along with extracellular matrix. In particular, fibroblasts are of significant interest as these cells are reprogrammed during tumorigenesis to become cancer‐associated fibroblasts (CAFs), which in turn support cancer cell growth. MicroRNAs (miRNAs) have been shown to be involved in this intercellular crosstalk in humans. To assess whether miRNAs are also involved in the activation of fibroblasts in dogs, we cocultured primary canine skin fibroblasts with the canine mast cell tumour cell line C2 directly or with C2‐derived exosomes, and measured differential abundance of selected miRNAs. Expression of the CAF markers alpha‐smooth muscle actin (ACTA2) and stanniocalcin 1 confirmed the activation of our fibroblasts after coculture. We show that fibroblasts displayed significant downregulation of miR‐27a and let‐7 family members. These changes correlated with significant upregulation of predicted target mRNAs. Furthermore, RNA interference knockdown of miR‐27a revealed that cyclin G1 (CCNG1) exhibited negative correlation at the mRNA and protein level, suggesting that CCNG1 is a target of miR‐27a in canine fibroblasts and involved in their activation. Importantly, miR‐27a knockdown itself resulted in fibroblast activation, as demonstrated by the formation of ACTA2 filaments. In addition, interleukin‐6 (IL‐6) was strongly induced in our fibroblasts when cocultured, indicating potential reciprocal signalling. Taken together, our findings are consistent with canine fibroblasts being reprogrammed into CAFs to further support cancer development and that downregulation of miR‐27a may play an important role in the tumour–microenvironment crosstalk.

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“…MiR-27b-3p and miR-218-5p were another two downregulated miRNAs in our case study that are reported for the first time in melanoma. MiR-27b-3p was also downregulated in lung cancer tissues [53] and in breast cancer tissues and cell lines, where it was associated with chemoresistance [54]. However, miR-27b-3p expression was increased in Dox-resistant anaplastic thyroid cancer (ATC) cells [55].…”

Section: Discussionmentioning

confidence: 99%

A preliminary study of microRNA expression in different types of primary melanoma

Gencia

Baderca

Avram

et al. 2019

Bosn J of Basic Med Sci

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MicroRNAs (miRNAs) have been proven to regulate the development and progression of cancer through various mechanisms. The aim of the present study was to compare miRNA expression between primary melanomas from different sites. We analyzed the expression of 84 miRNAs in 27 primary melanoma and 5 nevus formalin-fixed paraffin-embedded (FFPE) samples using the Human Cancer PathwayFinder miScript miRNA PCR Array. The FFPE samples were obtained from the archives of the Municipal Clinical Emergency Hospital of Timisoara and included 10 cutaneous melanomas, 10 uveal melanomas, 7 mucosal melanomas, and 5 cutaneous nevi. Out of 84 miRNAs, 11 miRNAs showed altered expression in all types of melanoma compared with the nevi. Among these, miR-155-5p, miR-9-5p, miR-142-5p, miR-19a-3p, miR-134-5p, and miR-301a-3p were upregulated, while miR-205-5p, miR-203a-3p, miR-27b-3p, miR-218-5p, and miR-23b-3p were downregulated. The highest similarity in miRNA expression pattern was found between uveal and mucosal melanoma groups, i.e., 15 miRNAs had altered expression in both groups. Overall, we identified several miRNAs with significantly altered expression in primary melanomas, including those reported for the first time in this type of cancer. Among them, mir-9-5p, mir-203a-3p, mir-19a-3p, mir-27b-3p, and mir-218-5p showed altered expression in all melanoma groups vs. nevus group. Further research should explore the potential of these miRNAs in melanoma.

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miR-27b-3p inhibits proliferation and potentially reverses multi-chemoresistance by targeting CBLB/GRB2 in breast cancer cells

Cited by 114 publications

References 43 publications

Downregulated miR‐27b promotes keratinocyte proliferation by targeting PLK2 in oral lichen planus

Downregulated miR‐27b promotes keratinocyte proliferation by targeting PLK2 in oral lichen planus

Deregulation of miR‐27a may contribute to canine fibroblast activation after coculture with a mast cell tumour cell line

A preliminary study of microRNA expression in different types of primary melanoma

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