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Research article
miR-200c inhibits the invasive activity of primary adamantinomatous craniopharyngioma cells
jianguo xu
Sichuan University West China Hospital
Corresponding Author
ORCiD: https://orcid.org/0000-0003-3623-4549
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This work is licensed under a CC BY 4.0 License. Read Full License
Backgrounds Craniopharyngiomas are benign epithelial tumors and difficult to complete due to the digitate brain infiltration. miR-200c has been studied in terms of development, stemness, epithelial-mesenchymal transition (EMT), and therapy resistance in many cancers. However, the role of miR-200c remains to be elucidated in adamantinomatous craniopharyngioma.
Methods Quantitative real-time polymerase chain reaction was used to evaluate the expression of miR-200c, ZEB1, ZEB2, and CTNNB1. Immunohistochemistry, Western blot, and immunofluorescence analyses were used to evaluate the expression of E-cadherin and β-catenin at the protein level. A Transwell assay was used to evaluate the invasiveness of ten primary craniopharyngioma cell.
Results miR-200c was significantly downregulated in adamantinomatous craniopharyngioma compared with papillary craniopharyngioma. Conversely, ZEB1, ZEB2, and CTNNB1 were overexpressed in adamantinomatous craniopharyngioma. Inhibition of miR-200c significantly promoted the invasion of primary adamantinomatous craniopharyngioma cells. Moreover, E-cadherin was overexpressed and β-catenin was downregulated in miR-200c mimic primary adamantinomatous craniopharyngioma cell culture.
Conclusion Our data demonstrated that miR-200c maybe reduce the invasive activity of adamantinomatous craniopharyngioma cells through E-cadherin/β-catenin. These findings suggest that the targets of miR-200c may regulate the EMT of adamantinomatous craniopharyngioma.
Keywords
craniopharyngioma, miR-200c, invasion, EMT, adamantinomatous craniopharyngioma
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This is a preprint. It has not completed peer review.
Research article
miR-200c inhibits the invasive activity of primary adamantinomatous craniopharyngioma cells
jianguo xu
Sichuan University West China Hospital
Corresponding Author
ORCiD: https://orcid.org/0000-0003-3623-4549
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
Version 1
Posted 23 Dec, 2019
No community comments so far
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Backgrounds Craniopharyngiomas are benign epithelial tumors and difficult to complete due to the digitate brain infiltration. miR-200c has been studied in terms of development, stemness, epithelial-mesenchymal transition (EMT), and therapy resistance in many cancers. However, the role of miR-200c remains to be elucidated in adamantinomatous craniopharyngioma.
Methods Quantitative real-time polymerase chain reaction was used to evaluate the expression of miR-200c, ZEB1, ZEB2, and CTNNB1. Immunohistochemistry, Western blot, and immunofluorescence analyses were used to evaluate the expression of E-cadherin and β-catenin at the protein level. A Transwell assay was used to evaluate the invasiveness of ten primary craniopharyngioma cell.
Results miR-200c was significantly downregulated in adamantinomatous craniopharyngioma compared with papillary craniopharyngioma. Conversely, ZEB1, ZEB2, and CTNNB1 were overexpressed in adamantinomatous craniopharyngioma. Inhibition of miR-200c significantly promoted the invasion of primary adamantinomatous craniopharyngioma cells. Moreover, E-cadherin was overexpressed and β-catenin was downregulated in miR-200c mimic primary adamantinomatous craniopharyngioma cell culture.
Conclusion Our data demonstrated that miR-200c maybe reduce the invasive activity of adamantinomatous craniopharyngioma cells through E-cadherin/β-catenin. These findings suggest that the targets of miR-200c may regulate the EMT of adamantinomatous craniopharyngioma.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5