{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,13]],"date-time":"2026-07-13T13:24:24Z","timestamp":1783949064973,"version":"3.55.0"},"reference-count":33,"publisher":"Termedia Sp. z.o.o.","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Pol J Pathol"],"abstract":"<jats:p>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. &lt;br \/&gt;\nHere, 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\u2032-UTR, and confirmed the combination of miR-328-3p and ANRIL and TSC1\/ULK2 3\u2032-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.&lt;br \/&gt;\nOur 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.<\/jats:p>","DOI":"10.5114\/pjp.2024.142177","type":"journal-article","created":{"date-parts":[[2024,8,20]],"date-time":"2024-08-20T05:26:22Z","timestamp":1724131582000},"page":"228-235","source":"Crossref","is-referenced-by-count":3,"title":["ANRIL regulates retinoblastoma progression via targeting autophagy by miR-328-3p\/TSC1\/ULK signaling"],"prefix":"10.5114","volume":"75","author":[{"given":"Yang","family":"Yang","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuezhi","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yanmei","family":"Fu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shuanglian","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaolong","family":"Yin","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"3061","published-online":{"date-parts":[[2024,8,12]]},"reference":[{"key":"ref-1689206","doi-asserted-by":"crossref","unstructured":"Dimaras H, Corson TW. 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Eur Rev Med Pharmacol Sci 2020; 24: 9256-9264."},{"key":"ref-1689218","doi-asserted-by":"crossref","unstructured":"Yang L, Zhang L, Lu L, Wang Y. lncRNA UCA1 increases proliferation and multidrug resistance of retinoblastoma cells through downregulating miR-513a-5p. DNA Cell Biol 2020; 39: 69-77.","DOI":"10.1089\/dna.2019.5063"},{"key":"ref-1689219","doi-asserted-by":"crossref","unstructured":"Kong Y, Hsieh CH, Alonso LC. ANRIL: a lncRNA at the CDKN2A\/B locus with roles in cancer and metabolic disease. Front Endocrinol 2018; 9: 405.","DOI":"10.3389\/fendo.2018.00405"},{"key":"ref-1689220","doi-asserted-by":"crossref","unstructured":"Sun LY, Li XJ, Sun YM, et al. LncRNA ANRIL regulates AML development through modulating the glucose metabolism pathway of AdipoR1\/AMPK\/SIRT1. Mol Cancer 2018; 17: 127.","DOI":"10.1186\/s12943-018-0879-9"},{"key":"ref-1689221","doi-asserted-by":"crossref","unstructured":"Kangarlouei R, Irani S, Noormohammadi Z, Memari F, Mirfakhraie R. ANRIL and ANRASSF1 long noncoding RNAs are upregulated in gastric cancer. J Cellular Biochem 2019; 120: 12544-12548.","DOI":"10.1002\/jcb.28520"},{"key":"ref-1689222","doi-asserted-by":"crossref","unstructured":"Yin X, Liao Y, Xiong W, et al. Hypoxia-induced lncRNA ANRIL promotes cisplatin resistance in retinoblastoma cells through regulating ABCG2 expression. Clin Exp Pharmacol Physiol 2020; 47: 1049-1057.","DOI":"10.1111\/1440-1681.13279"},{"key":"ref-1689223","doi-asserted-by":"crossref","unstructured":"Galluzzi L, Green DR. Autophagy-independent functions of the autophagy machinery. Cell 2019; 177: 1682-1699.","DOI":"10.1016\/j.cell.2019.05.026"},{"key":"ref-1689224","unstructured":"Yao L, Yang L, Song H, Liu TG, Yan H. Silencing of lncRNA XIST suppresses proliferation and autophagy and enhances vincristine sensitivity in retinoblastoma cells by sponging miR-204-5p. Eur Rev Med Pharmacol Sci 2020; 24: 3526-3537."},{"key":"ref-1689225","doi-asserted-by":"crossref","unstructured":"Yang M, Wei W. Long non-coding RNAs in retinoblastoma. Pathol Res Practice 2019; 215: 152435.","DOI":"10.1016\/j.prp.2019.152435"},{"key":"ref-1689226","doi-asserted-by":"crossref","unstructured":"Al-Bari MAA, Xu P. Molecular regulation of autophagy machinery by mTOR-dependent and -independent pathways. Ann N York Acad Sci 2020; 1467: 3-20.","DOI":"10.1111\/nyas.14305"},{"key":"ref-1689227","doi-asserted-by":"crossref","unstructured":"Gao S, Chu Q, Liu X, et al. Long noncoding RNA HEIH promotes proliferation, migration and invasion of retinoblastoma cells through miR-194-5p\/WEE1 axis. 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