MicroRNA-21 expression, serum tumor markers, and immunohistochemistry in canine mammary tumors

Abstract Background: Canine mammary tumors (CMTs) are one of the most common malignancies in dogs and are associated with significant mortality. Serum tumor markers and non-coding microRNAs have recently gained widespread popularity in human oncology studies. We aimed to investigate the expression of microRNA-21 (miR21), changes in serum tumor markers (CEA and CA 15-3), and immunohistochemistry in CMTs diagnosed by clinical examination, radiology, and histopathology. This study enrolled 17 female dogs: 10 with mammary tumors and seven controls without tumors. Blood samples were collected to measure miR-21, CEA, and CA 15-3, and histological samples were prepared for histological grading and immunohistochemistry. Results: CA 15-3 was elevated in all animals, whereas CEA levels showed no change compared with controls. miR-21 was upregulated 12.84-fold in animals with CMT. The most frequently recorded CMT was mixed type. Myoepithelial cells were identified by P63 immunoreactivity, but not SMA. High expression of miR-21 was observed with positive vimentin immunoreactivity, indicating a mesenchymal origin of the tumor cells. Conclusion: The present study showed that miR-21 was elevated to a greater extent than CA 15-3 (12.84-fold vs. threefold). Mixed-type tumors with positive vimentin immunoreactivity showed the highest miR-21 levels. These findings support the hypothesis that miR-21 may be a more sensitive, noninvasive indicator for CMT.

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Faculty Opinions recommendation of A Comparison of Fresh Frozen vs. Formalin-Fixed, Paraffin-Embedded Specimens of Canine Mammary Tumors via Branched-DNA Assay.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.726361618.793528010 ◽

2017 ◽

Author(s):

Alexandre Alanio

Keyword(s):

Mammary Tumors ◽

Dna Assay ◽

Branched Dna ◽

Canine Mammary Tumors ◽

Formalin Fixed Paraffin ◽

Formalin Fixed Paraffin Embedded ◽

Fresh Frozen ◽

Formalin Fixed

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Serum Tumor Markers in Stage I-II Breast Cancer

Medicinal Chemistry ◽

10.2174/1573406412666151116144520 ◽

2016 ◽

Vol 12 (3) ◽

pp. 285-289 ◽

Cited By ~ 5

Author(s):

Renato Tozzoli ◽

Federica D';Aurizio ◽

Flavio Falcomer ◽

Stefano M.M. Basso ◽

Franco Lumachi

Keyword(s):

Breast Cancer ◽

Tumor Markers ◽

Stage I ◽

Serum Tumor Markers

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Overexpression of Mucin 1 Suppresses the Therapeutical Efficacy of Disulfiram against Canine Mammary Tumor

Animals ◽

10.3390/ani11010037 ◽

2020 ◽

Vol 11 (1) ◽

pp. 37

Author(s):

Ying Zhao ◽

Zixiang Lin ◽

Zhaoyan Lin ◽

Chaoyu Zhou ◽

Gang Liu ◽

...

Keyword(s):

Mammary Tumor ◽

Mammary Tumors ◽

Expression Level ◽

Canine Mammary Tumor ◽

Wild Type ◽

Mucin 1 ◽

Mammary Tumor Cell ◽

Mammary Tumor Cell Line ◽

Canine Mammary Tumors ◽

Wild Type Control

Mucin 1 (MUC1), a transmembrane protein, is closely associated with the malignancy and metastasis of canine mammary tumors; however, the role of overexpressed MUC1 in the development of cancer cells and response to drug treatment remains unclear. To address this question, we developed a new canine mammary tumor cell line, CIPp-MUC1, with an elevated expression level of MUC1. In vitro studies showed that CIPp-MUC1 cells are superior in proliferation and migration than wild-type control, which was associated with the upregulation of PI3K, p-Akt, mTOR, Bcl-2. In addition, overexpression of MUC1 in CIPp-MUC1 cells inhibited the suppressing activity of disulfiram on the growth and metastasis of tumor cells, as well as inhibiting the pro-apoptotic effect of disulfiram. In vivo studies, on the other side, showed more rapid tumor growth and stronger resistance to disulfiram treatment in CIPp-MUC1 xenograft mice than in wild-type control. In conclusion, our study demonstrated the importance of MUC1 in affecting the therapeutical efficiency of disulfiram against canine mammary tumors, indicating that the expression level of MUC1 should be considered for clinical use of disulfiram or other drugs targeting PI3K/Akt pathway.

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