LINC01278 Induces Autophagy to Inhibit Tumour Progression by Suppressing the mTOR Signalling Pathway

Author:

Liu Bo12,Yao Xueting3,Zhang Chaoyang4ORCID,Li Wenzhe12,Wang Yanan12,Liao Qianling12,Li Ziwei12,Huang Qinying12,Zhang Yanchen12,Wu Wencan12ORCID

Affiliation:

1. State Key Laboratory of Ophthalmology, Optometry, And Vision Science, Wenzhou Medical University, Wenzhou, China

2. The Eye Hospital, School of Ophthalmology & Optometry, Wenzhou Medical University, Wenzhou, China

3. Department of Laboratory Medicine, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China

4. Department of General Surgery, The First Affiliated Hospital of Anhui Medical University, Hefei, China

Abstract

Uveal melanoma (UM) is an aggressive intraocular malignant tumour that is closely related to autophagic dysfunction. We aimed to identify autophagy-related long noncoding RNAs (lncRNAs) to elucidate the molecular mechanism of UM. Here, we show that LINC01278 is a new potential biomarker with clinical prognostic value in UM through bioinformatics analysis. Application of an autophagy inhibitor (3-MA) and an autophagy agonist (MG-132) indicated that LINC01278 can inhibit UM cell proliferation, migration, and invasion by inducing autophagy. A xenograft nude mouse model was used to examine the tumorigenesis of UM cells in vivo. Mechanistically, LINC01278 can inhibit the mTOR signalling pathway to activate autophagy, as shown by experiments with an mTOR agonist (MHY1485) and mTOR inhibitor (rapamycin) treatment. Our findings indicate that LINC01278 functions as a tumour suppressor by inhibiting the mTOR signalling pathway to induce autophagy. Targeting the LINC01278-mTOR axis might be a novel and promising therapeutic approach for UM.

Funder

Key R&D Program of Wenzhou Eye Hospital

Publisher

Hindawi Limited

Subject

Cell Biology,Aging,General Medicine,Biochemistry

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