MiR‐577 suppresses epithelial‐mesenchymal transition and metastasis of breast cancer by targeting Rab25

Background MicroRNAs can act as both tumor suppressor genes and oncogenes and participate in cell proliferation, metastasis, and apoptosis. Low levels of miR‐577 are found in several cancers, for example, thyroid carcinoma, glioblastoma, and hepatocellular carcinoma. The aim of this study was to inv...

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Veröffentlicht in:Thoracic cancer 2018-04, Vol.9 (4), p.472-479
Hauptverfasser: Yin, Chonggao, Mou, Qingjie, Pan, Xinting, Zhang, Guoxin, Li, Hongli, Sun, Yunbo
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container_end_page 479
container_issue 4
container_start_page 472
container_title Thoracic cancer
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creator Yin, Chonggao
Mou, Qingjie
Pan, Xinting
Zhang, Guoxin
Li, Hongli
Sun, Yunbo
description Background MicroRNAs can act as both tumor suppressor genes and oncogenes and participate in cell proliferation, metastasis, and apoptosis. Low levels of miR‐577 are found in several cancers, for example, thyroid carcinoma, glioblastoma, and hepatocellular carcinoma. The aim of this study was to investigate the effect of miR‐577 on breast cancer (BC). Methods The relative level of miR‐577 in 120 BC tissues and cells was detected by real‐time PCR. MDA‐MB‐231 cells with upregulated miR‐577 and MCF‐7 cells with downregulated miR‐577 were established. Transwell invasion assays were used to examine the invasiveness of cells. Epithelial‐mesenchymal transition (EMT) markers were evaluated by immunofluorescence and Western blot. Targeted combinations of miR‐577 and Rab25 were analyzed by luciferase assays. Xenograft models were used to examine the effect of miR‐577 on BC metastasis. Results MiR‐577 expression was significantly suppressed in BC tissues. Tumor size, tumor stage, and lymphatic metastasis were attributed to miR‐577 expression. Moreover, miR‐577 overexpression strongly inhibited the invasiveness and EMT of BC cells in vitro. MiR‐577 directly regulated Rab25 in BC. Rab25 upregulation by miR‐577 decreased the levels of E‐cadherin and increased the levels of Vimentin. Notably, Rab25 knockdown inhibited BC invasion; however, an increase in Rab25 counteracted the invasive effect of miR‐577 in BC. Conclusion Results indicated that miR‐577 suppressed EMT by inhibiting Rab25 expression in BC. MiR‐577 and Rab25 are considered potential targets of BC treatment.
doi_str_mv 10.1111/1759-7714.12612
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Low levels of miR‐577 are found in several cancers, for example, thyroid carcinoma, glioblastoma, and hepatocellular carcinoma. The aim of this study was to investigate the effect of miR‐577 on breast cancer (BC). Methods The relative level of miR‐577 in 120 BC tissues and cells was detected by real‐time PCR. MDA‐MB‐231 cells with upregulated miR‐577 and MCF‐7 cells with downregulated miR‐577 were established. Transwell invasion assays were used to examine the invasiveness of cells. Epithelial‐mesenchymal transition (EMT) markers were evaluated by immunofluorescence and Western blot. Targeted combinations of miR‐577 and Rab25 were analyzed by luciferase assays. Xenograft models were used to examine the effect of miR‐577 on BC metastasis. Results MiR‐577 expression was significantly suppressed in BC tissues. Tumor size, tumor stage, and lymphatic metastasis were attributed to miR‐577 expression. Moreover, miR‐577 overexpression strongly inhibited the invasiveness and EMT of BC cells in vitro. MiR‐577 directly regulated Rab25 in BC. Rab25 upregulation by miR‐577 decreased the levels of E‐cadherin and increased the levels of Vimentin. Notably, Rab25 knockdown inhibited BC invasion; however, an increase in Rab25 counteracted the invasive effect of miR‐577 in BC. Conclusion Results indicated that miR‐577 suppressed EMT by inhibiting Rab25 expression in BC. MiR‐577 and Rab25 are considered potential targets of BC treatment.</description><identifier>ISSN: 1759-7706</identifier><identifier>EISSN: 1759-7714</identifier><identifier>DOI: 10.1111/1759-7714.12612</identifier><identifier>PMID: 29524309</identifier><language>eng</language><publisher>Melbourne: John Wiley &amp; Sons Australia, Ltd</publisher><subject>Aged ; Analysis ; Apoptosis ; Breast cancer ; Breast Neoplasms - genetics ; Breast Neoplasms - pathology ; Cell cycle ; Cell growth ; Cell Movement - genetics ; Cell Proliferation - genetics ; Colorectal cancer ; Deoxyribonucleic acid ; DNA ; Epithelial-Mesenchymal Transition - genetics ; epithelial‐mesenchymal transition ; Female ; Gene expression ; Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; Gliomas ; Humans ; Immunoglobulins ; Liver cancer ; Lymphatic Metastasis ; MCF-7 Cells ; Membranes ; Metastasis ; MicroRNA ; MicroRNAs ; MicroRNAs - genetics ; Middle Aged ; MiR‐577 ; Neoplasm Invasiveness - genetics ; Neoplasm Invasiveness - pathology ; Original ; rab GTP-Binding Proteins - genetics ; Rab25 ; Stem cells ; Studies ; Thyroid cancer ; Thyroid diseases ; Tumors</subject><ispartof>Thoracic cancer, 2018-04, Vol.9 (4), p.472-479</ispartof><rights>2018 The Authors. Thoracic Cancer published by China Lung Oncology Group and John Wiley &amp; Sons Australia, Ltd</rights><rights>2018 The Authors. Thoracic Cancer published by China Lung Oncology Group and John Wiley &amp; Sons Australia, Ltd.</rights><rights>COPYRIGHT 2018 John Wiley &amp; Sons, Inc.</rights><rights>2018. This work is published under http://creativecommons.org/licenses/by-nc/4.0/ (the “License”). 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Low levels of miR‐577 are found in several cancers, for example, thyroid carcinoma, glioblastoma, and hepatocellular carcinoma. The aim of this study was to investigate the effect of miR‐577 on breast cancer (BC). Methods The relative level of miR‐577 in 120 BC tissues and cells was detected by real‐time PCR. MDA‐MB‐231 cells with upregulated miR‐577 and MCF‐7 cells with downregulated miR‐577 were established. Transwell invasion assays were used to examine the invasiveness of cells. Epithelial‐mesenchymal transition (EMT) markers were evaluated by immunofluorescence and Western blot. Targeted combinations of miR‐577 and Rab25 were analyzed by luciferase assays. Xenograft models were used to examine the effect of miR‐577 on BC metastasis. Results MiR‐577 expression was significantly suppressed in BC tissues. Tumor size, tumor stage, and lymphatic metastasis were attributed to miR‐577 expression. Moreover, miR‐577 overexpression strongly inhibited the invasiveness and EMT of BC cells in vitro. MiR‐577 directly regulated Rab25 in BC. Rab25 upregulation by miR‐577 decreased the levels of E‐cadherin and increased the levels of Vimentin. Notably, Rab25 knockdown inhibited BC invasion; however, an increase in Rab25 counteracted the invasive effect of miR‐577 in BC. Conclusion Results indicated that miR‐577 suppressed EMT by inhibiting Rab25 expression in BC. 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Low levels of miR‐577 are found in several cancers, for example, thyroid carcinoma, glioblastoma, and hepatocellular carcinoma. The aim of this study was to investigate the effect of miR‐577 on breast cancer (BC). Methods The relative level of miR‐577 in 120 BC tissues and cells was detected by real‐time PCR. MDA‐MB‐231 cells with upregulated miR‐577 and MCF‐7 cells with downregulated miR‐577 were established. Transwell invasion assays were used to examine the invasiveness of cells. Epithelial‐mesenchymal transition (EMT) markers were evaluated by immunofluorescence and Western blot. Targeted combinations of miR‐577 and Rab25 were analyzed by luciferase assays. Xenograft models were used to examine the effect of miR‐577 on BC metastasis. Results MiR‐577 expression was significantly suppressed in BC tissues. Tumor size, tumor stage, and lymphatic metastasis were attributed to miR‐577 expression. Moreover, miR‐577 overexpression strongly inhibited the invasiveness and EMT of BC cells in vitro. MiR‐577 directly regulated Rab25 in BC. Rab25 upregulation by miR‐577 decreased the levels of E‐cadherin and increased the levels of Vimentin. Notably, Rab25 knockdown inhibited BC invasion; however, an increase in Rab25 counteracted the invasive effect of miR‐577 in BC. Conclusion Results indicated that miR‐577 suppressed EMT by inhibiting Rab25 expression in BC. MiR‐577 and Rab25 are considered potential targets of BC treatment.</abstract><cop>Melbourne</cop><pub>John Wiley &amp; Sons Australia, Ltd</pub><pmid>29524309</pmid><doi>10.1111/1759-7714.12612</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0001-6333-2270</orcidid><oa>free_for_read</oa></addata></record>
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subjects Aged
Analysis
Apoptosis
Breast cancer
Breast Neoplasms - genetics
Breast Neoplasms - pathology
Cell cycle
Cell growth
Cell Movement - genetics
Cell Proliferation - genetics
Colorectal cancer
Deoxyribonucleic acid
DNA
Epithelial-Mesenchymal Transition - genetics
epithelial‐mesenchymal transition
Female
Gene expression
Gene Expression Regulation, Neoplastic
Gene Knockdown Techniques
Gliomas
Humans
Immunoglobulins
Liver cancer
Lymphatic Metastasis
MCF-7 Cells
Membranes
Metastasis
MicroRNA
MicroRNAs
MicroRNAs - genetics
Middle Aged
MiR‐577
Neoplasm Invasiveness - genetics
Neoplasm Invasiveness - pathology
Original
rab GTP-Binding Proteins - genetics
Rab25
Stem cells
Studies
Thyroid cancer
Thyroid diseases
Tumors
title MiR‐577 suppresses epithelial‐mesenchymal transition and metastasis of breast cancer by targeting Rab25
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