LINC01541 Functions as a ceRNA to Modulate the Wnt/β-Catenin Pathway by Decoying miR-506-5p in Endometriosis
Endometriosis is one of the most common gynecological diseases that adversely effects the lives of women. Our previous studies showed that LINC01541 plays a key role in 17β-estradiol (17β-E2)-stimulated endometrial stromal cells (ESCs); however, the mechanism by which LINC01541 exerts if effects requires further elaboration. Here, we report that LINC01541 serves to reduce the bioavailability of miR-506-5p by acting as a molecular sponge. Samples of control endometrial tissue and ectopic endometrial tissue were obtained from 10 healthy volunteers and 18 patients with endometriosis, respectively, and the levels of LINC01541 and miR-506-5p expressions in those tissues were measured. The relationship between LINC01541 and miR-506-5p was verified in 17β-E2-stimulated ESCs. Overexpression or silencing of miR-506-5p in ESCs was performed explore its role in endometriosis, and we also investigated whether WNT inhibitory factor 1 (WIF1) might be a target gene of miR-506-5p. Our results showed that LINC01541 was expressed at low levels and miR-506-5p was expressed at high levels in ectopic tissues. LINC01541 expression was negatively correlated with miR-506-5p expression. We also found that miR-506-5p activated the Wnt/β-catenin pathway by inhibiting WIF1 expression, and thereby induced the proliferation, migration, and invasion of ESCs. Furthermore, silencing of miR-506-5p promoted apoptosis and suppressed the proliferation of 17β-E2-treated ESCs. Overexpression of miR-506-5p could reverse the inhibitory effect of LINC01541 in endometriosis. In summary, this study found that in endometriosis, LINC01541 functions as a ceRNA that modulates the Wnt/β-catenin pathway by decoying miR-506-5p.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2021 |
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| Erschienen: |
2021 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:28 |
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| Enthalten in: |
Reproductive sciences (Thousand Oaks, Calif.) - 28(2021), 3 vom: 24. März, Seite 665-674 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Mai, Hong [VerfasserIn] |
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| Links: |
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| Anmerkungen: |
Date Completed 23.11.2021 Date Revised 23.11.2021 published: Print-Electronic Citation Status MEDLINE |
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| doi: |
10.1007/s43032-020-00295-3 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM314066470 |
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| 100 | 1 | |a Mai, Hong |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a LINC01541 Functions as a ceRNA to Modulate the Wnt/β-Catenin Pathway by Decoying miR-506-5p in Endometriosis |
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| 500 | |a Citation Status MEDLINE | ||
| 520 | |a Endometriosis is one of the most common gynecological diseases that adversely effects the lives of women. Our previous studies showed that LINC01541 plays a key role in 17β-estradiol (17β-E2)-stimulated endometrial stromal cells (ESCs); however, the mechanism by which LINC01541 exerts if effects requires further elaboration. Here, we report that LINC01541 serves to reduce the bioavailability of miR-506-5p by acting as a molecular sponge. Samples of control endometrial tissue and ectopic endometrial tissue were obtained from 10 healthy volunteers and 18 patients with endometriosis, respectively, and the levels of LINC01541 and miR-506-5p expressions in those tissues were measured. The relationship between LINC01541 and miR-506-5p was verified in 17β-E2-stimulated ESCs. Overexpression or silencing of miR-506-5p in ESCs was performed explore its role in endometriosis, and we also investigated whether WNT inhibitory factor 1 (WIF1) might be a target gene of miR-506-5p. Our results showed that LINC01541 was expressed at low levels and miR-506-5p was expressed at high levels in ectopic tissues. LINC01541 expression was negatively correlated with miR-506-5p expression. We also found that miR-506-5p activated the Wnt/β-catenin pathway by inhibiting WIF1 expression, and thereby induced the proliferation, migration, and invasion of ESCs. Furthermore, silencing of miR-506-5p promoted apoptosis and suppressed the proliferation of 17β-E2-treated ESCs. Overexpression of miR-506-5p could reverse the inhibitory effect of LINC01541 in endometriosis. In summary, this study found that in endometriosis, LINC01541 functions as a ceRNA that modulates the Wnt/β-catenin pathway by decoying miR-506-5p | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a 17β-estradiol | |
| 650 | 4 | |a Endometrial stromal cells | |
| 650 | 4 | |a Endometriosis | |
| 650 | 4 | |a lncRNA | |
| 650 | 4 | |a microRNA | |
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| 700 | 1 | |a Wei, Yeping |e verfasserin |4 aut | |
| 700 | 1 | |a Yin, Yan |e verfasserin |4 aut | |
| 700 | 1 | |a Huang, Yifang |e verfasserin |4 aut | |
| 700 | 1 | |a Huang, Shijin |e verfasserin |4 aut | |
| 700 | 1 | |a Liao, Yan |e verfasserin |4 aut | |
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