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FEAT enhances INSL3 expression in testicular Leydig cells.
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- Author(s): Li Y;Li Y;Li Y;Li Y; Kobayashi K; Kobayashi K; Murayama K; Murayama K; Kawahara K; Kawahara K; Shima Y; Shima Y; Suzuki A; Suzuki A; Suzuki A; Tani K; Tani K; Tani K; Takahashi A; Takahashi A; Takahashi A; Takahashi A; Takahashi A; Takahashi A
- Source:
Genes to cells : devoted to molecular & cellular mechanisms [Genes Cells] 2018 Nov; Vol. 23 (11), pp. 952-962. Date of Electronic Publication: 2018 Oct 02.- Publication Type:
Journal Article- Language:
English - Source:
- Additional Information
- Source: Publisher: Blackwell Science Ltd Country of Publication: England NLM ID: 9607379 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1365-2443 (Electronic) Linking ISSN: 13569597 NLM ISO Abbreviation: Genes Cells Subsets: MEDLINE
- Publication Information: Original Publication: Oxford, UK : Blackwell Science Ltd., 1996-
- Subject Terms: Cryptorchidism/*metabolism ; Insulin/*metabolism ; Leydig Cells/*metabolism ; Methyltransferases/*metabolism ; Proteins/*metabolism ; Testis/*metabolism; Animals ; Cell Movement ; Cryptorchidism/pathology ; Insulin/genetics ; Leydig Cells/cytology ; Male ; Mice ; Proteins/genetics ; Testis/cytology ; Transcriptional Activation
- Abstract: FEAT, the protein encoded by methyltransferase-like 13 (METTL13), is aberrantly upregulated in most human cancers and potently drives tumorigenesis in vivo; however, its role in normal tissues remains elusive. Immunoblotting has displayed weak FEAT expression in normal human tissues, including the testis. Here, we found that FEAT is expressed in fetal and adult Leydig cells in the testis. FEAT knockdown using siRNA increased primary cilia formation in MA-10 Leydig tumor cells, accompanied by enhanced 5' adenosine monophosphate-activated protein kinase (AMPK) activation. Immunofluorescence analyses of FEAT-silenced MA-10 cells showed diminished insulin-like factor 3 (INSL3) expression. A male Mettl13 +/- mouse developed bilateral intraabdominal cryptorchidism, suggesting defective INSL3 production by fetal Leydig cells. Leydig cells from the mouse showed markedly decreased INSL3 protein by immunohistochemistry. Together, these results suggest that FEAT facilitates the INSL3 production in testicular Leydig cells that is essential for transabdominal testis migration.
(© 2018 Molecular Biology Society of Japan and John Wiley & Sons Australia, Ltd.) - Grant Information: Ube Foundation; Ministry of Education, Culture, Sports, Science and Technology; Chiyoda Mutual Life Foundation; 16K07141 Japan Society for the Promotion of Science; 25430132 Japan Society for the Promotion of Science
- Accession Number: 0 (Insulin)
0 (Leydig insulin-like protein)
0 (Proteins)
EC 2.1.1.- (EEF1AKNMT protein, human)
EC 2.1.1.- (Methyltransferases) - Publication Date: Date Created: 20180905 Date Completed: 20190125 Latest Revision: 20210301
- Publication Date: 20240104
- Accession Number: 10.1111/gtc.12644
- Accession Number: 30178547
- Source:
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