PMID- 28901408 OWN - NLM STAT- MEDLINE DCOM- 20180611 LR - 20180816 IS - 1791-3004 (Electronic) IS - 1791-2997 (Linking) VI - 16 IP - 5 DP - 2017 Nov TI - MicroRNA‑382 inhibits cell proliferation and invasion of retinoblastoma by targeting BDNF‑mediated PI3K/AKT signalling pathway. PG - 6428-6436 LID - 10.3892/mmr.2017.7396 [doi] AB - It has previously been demonstrated that multiple microRNAs (miRNAs or miRs) are aberrantly expressed in retinoblastoma (RB) and contribute to RB initiation and progression. miR‑382 has been revealed to be aberrantly expressed and therefore exhibits a key role in the progression of various types of cancer. However, the expression pattern, functional roles and underlying molecular mechanism of miR‑382 in RB remain unknown. The present study investigated the expression levels of miR‑382 and its effects on RB cells and the underlying regulatory mechanism of its action. It was demonstrated that miR‑382 was downregulated in RB tissues and cell lines. Upregulation of miR‑382 inhibited RB cell proliferation and invasion in vitro. Additionally, brain‑derived neurotrophic factor (BDNF) was identified as a novel target of miR‑382 in RB. BDNF was upregulated in RB tissues and negatively associated with miR‑382 expression levels. Furthermore, BDNF overexpression rescued the tumour‑suppressing effects on RB cells induced by miR‑382. miR‑382 inactivated the phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signalling pathway in RB. These findings suggested that miR‑382 serves as a tumour suppressor in RB, in part, by targeting the BDNF‑mediated PI3K/AKT signalling pathway. The results of the present study suggest a potential therapeutic strategy for treating RB patients in the future. FAU - Song, Dan AU - Song D AD - Department of Ophthalmology, Beijing Tsinghua Changgung Hospital, School of Clinical Medicine, Tsinghua University, Beijing 102218, P.R. China. FAU - Diao, Jiandong AU - Diao J AD - Department of Oncology and Hematology, China‑Japan Union Hospital of Jilin University, Changchun, Jilin 130033, P.R. China. FAU - Yang, Yongjing AU - Yang Y AD - Department of Thoracic Oncology, Jilin Cancer Hospital, Changchun, Jilin 130012, P.R. China. FAU - Chen, Yahong AU - Chen Y AD - Department of Colorectal Surgery, China‑Japan Union Hospital of Jilin University, Changchun, Jilin 130033, P.R. China. LA - eng PT - Journal Article DEP - 20170829 PL - Greece TA - Mol Med Rep JT - Molecular medicine reports JID - 101475259 RN - 0 (Brain-Derived Neurotrophic Factor) RN - 0 (Drug Combinations) RN - 0 (Laminin) RN - 0 (MIRN382 microRNA, human) RN - 0 (MicroRNAs) RN - 0 (Oligoribonucleotides) RN - 0 (Proteoglycans) RN - 119978-18-6 (matrigel) RN - 7171WSG8A2 (BDNF protein, human) RN - 9007-34-5 (Collagen) RN - EC 1.13.12.- (Luciferases) RN - EC 2.7.1.- (Phosphatidylinositol 3-Kinases) RN - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt) SB - IM MH - Apoptosis/genetics MH - Base Sequence MH - Binding Sites MH - Brain-Derived Neurotrophic Factor/*genetics/metabolism MH - Case-Control Studies MH - Cell Line, Tumor MH - Cell Movement MH - Cell Proliferation MH - Collagen/chemistry MH - Drug Combinations MH - *Gene Expression Regulation, Neoplastic MH - Genes, Reporter MH - Humans MH - Laminin/chemistry MH - Luciferases/genetics/metabolism MH - MicroRNAs/agonists/*genetics/metabolism MH - Molecular Mimicry MH - Oligoribonucleotides/genetics/metabolism MH - Phosphatidylinositol 3-Kinases/*genetics/metabolism MH - Proteoglycans/chemistry MH - Proto-Oncogene Proteins c-akt/*genetics/metabolism MH - Retinal Neoplasms/*genetics/metabolism/pathology/surgery MH - Retinoblastoma/*genetics/metabolism/pathology/surgery MH - Signal Transduction EDAT- 2017/09/14 06:00 MHDA- 2018/06/12 06:00 CRDT- 2017/09/14 06:00 PHST- 2017/03/06 00:00 [received] PHST- 2017/08/16 00:00 [accepted] PHST- 2017/09/14 06:00 [pubmed] PHST- 2018/06/12 06:00 [medline] PHST- 2017/09/14 06:00 [entrez] AID - 10.3892/mmr.2017.7396 [doi] PST - ppublish SO - Mol Med Rep. 2017 Nov;16(5):6428-6436. doi: 10.3892/mmr.2017.7396. Epub 2017 Aug 29.