ANRIL regulates retinoblastoma progression via targeting autophagy by miR-328-3p/TSC1/ULK signaling
Retinoblastoma is the most common primary intraocular malignancy of childhood. The aim of our study was to investigate the role and regulatory mechanism of the long non-coding RNA ANRIL in retinoblastoma. Here, our data demonstrated that ANRIL overexpression inhibited miR-328-3p expression, but pr...
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| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Termedia Publishing House
2024-08-01
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| Series: | Polish Journal of Pathology |
| Subjects: | |
| Online Access: | https://www.termedia.pl/ANRIL-regulates-retinoblastoma-progression-via-targeting-autophagy-by-miR-328-3p-TSC1-ULK-signaling,55,54604,1,1.html |
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| Summary: | Retinoblastoma is the most common primary intraocular malignancy of childhood. The aim of our study was to investigate the role and regulatory mechanism of the long non-coding RNA ANRIL in retinoblastoma.
Here, our data demonstrated that ANRIL overexpression inhibited miR-328-3p expression, but promoted expression of autophagy-related proteins (LC3B, ATG5, and BECN1). Then we predicted the binding sites for ANRIL with miR-328-3p, and for miR-328 3p with TSC1/ULK2 3′-UTR, and confirmed the combination of miR-328-3p and ANRIL and TSC1/ULK2 3′-UTR. Importantly, the data showed that ANRIL overexpression promoted TSC1 and ULK2 expression, and inhibited the phosphorylation of mTOR. Finally, our results indicated that ANRIL overexpression facilitated Y79 cell proliferation and cisplatin-induced apoptosis.
Our results indicated that ANRIL promoted the proliferation and cisplatin resistance of Y79 cells through activating autophagy by promoting TSC1/ULK2 ex- pression via acting as a miR-328-3p sponge. |
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| ISSN: | 1233-9687 2084-9869 |