The
retinoblastoma is the most common intraocular malignant
tumor in infants and children; it is one of the deadliest forms of
cancer due to its limited sensitivity to
chemotherapy and
radiotherapy. In several
cancers, chemoresistance is associated with autophagy induction. Non-coding RNAs, including long non-coding RNAs (
lncRNA) and
microRNAs (
miRNAs) have been reported to regulate physiological activities of the cells, including proliferation, apoptosis, migration, as well as autophagy. MALAT1, a well-established
lncRNA acts as an oncogene, promotes
cancer proliferation, and
metastasis via the stimulation of autophagy. In addition to MALAT1, miR-124, a known
tumor suppressor, has also been reported to regulate cell apoptosis and autophagy in dopaminergic neurons. In the present study, we investigated the roles of MALAT1 and miR-124 in the regulation of
retinoblastoma cell autophagy through evaluating the changes of
autophagy-related proteins. Through direct targeting miR-124, MALAT1 promotes
retinoblastoma cell autophagy. Further, we investigated whether
Syntaxin 17 (STX17), a
Soluble NSF Attachment Protein receptor (SNARE) of the autophagosome, is involved in MALAT1/miR-124 regulation of
retinoblastoma cell autophagy, and the underlying mechanism. Taken together, we provided novel experimental and theoretical basis for regulation of
retinoblastoma cell autophagy, and potential direction of dealing with autophagy-induced chemoresistance of
retinoblastoma, which need further in-depth study.