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Updated: Aug 12, 2025

Exploring the Regulation of Lipid Droplet Catabolism through Lipophagy
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Exploring the Regulation of Lipid Droplet Catabolism through Lipophagy

Published on: January 31, 2025

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

Bo Liu1,2, Xueting Yao3, Chaoyang Zhang4

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

Oxidative Medicine and Cellular Longevity
|January 30, 2023
PubMed

Insights

LINC01278, a long noncoding RNA, suppresses uveal melanoma (UM) by activating autophagy via the mTOR pathway. This discovery offers a potential new therapeutic target for this aggressive eye cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Uveal melanoma (UM) is an aggressive intraocular tumor linked to impaired autophagy.
  • Identifying novel molecular mechanisms and biomarkers is crucial for UM treatment.

Purpose of the Study:

  • To identify autophagy-related long noncoding RNAs (lncRNAs) involved in UM.
  • To elucidate the molecular mechanism of LINC01278 in UM progression.

Main Methods:

  • Bioinformatics analysis to identify potential lncRNA biomarkers.
  • In vitro experiments using autophagy inhibitors/agonists (3-MA, MG-132) to assess LINC01278 function.
  • In vivo studies using a xenograft nude mouse model.
  • Experiments with mTOR pathway modulators (MHY1485, rapamycin).

Main Results:

  • LINC01278 was identified as a potential prognostic biomarker for UM.
  • LINC01278 inhibits UM cell proliferation, migration, and invasion by inducing autophagy.
  • LINC01278 suppresses tumor growth in vivo.
  • LINC01278 activates autophagy by inhibiting the mTOR signaling pathway.

Conclusions:

  • LINC01278 acts as a tumor suppressor in UM by inducing autophagy through mTOR pathway inhibition.
  • Targeting the LINC01278-mTOR axis presents a promising therapeutic strategy for UM.

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