This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Research article
jianguo xu
Sichuan University West China Hospital
Corresponding Author
ORCiD: https://orcid.org/0000-0003-3623-4549
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.
Keywords
craniopharyngioma, miR-200c, invasion, EMT, adamantinomatous craniopharyngioma
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This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Research article
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
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