A Yin-Yang 1/miR-30a regulatory circuit modulates autophagy in pancreatic cancer cells

Autophagy is a highly regulated biological process that mediates the degradation of intracellular components. It is required for tumor cell metabolism and homeostasis. Yin-Yang 1 (YY1) has been reported to be involved in autophagy in several carcinomas. However, its role in autophagy in pancreatic c...

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Bibliographic Details
Published in:Journal of translational medicine 2017-10, Vol.15 (1), p.211-211, Article 211
Main Authors: Yang, Chuang, Zhang, Jing-Jing, Peng, Yun-Peng, Zhu, Yi, Yin, Ling-Di, Wei, Ji-Shu, Gao, Wen-Tao, Jiang, Kui-Rong, Miao, Yi
Format: Article
Language:English
Subjects:
Apoptosis
Autophagy
Binding sites
Biotechnology
Cancer cells
Cancer therapies
Care and treatment
Chromatin
Diagnosis
Gene expression
Genomes
Kinases
MicroRNA
MicroRNAs
miR-30a
Pancreatic cancer
Phagocytosis
Physiological aspects
Proteins
Studies
Target recognition
Transcription factors
Tumorigenesis
YY1
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Summary:Autophagy is a highly regulated biological process that mediates the degradation of intracellular components. It is required for tumor cell metabolism and homeostasis. Yin-Yang 1 (YY1) has been reported to be involved in autophagy in several carcinomas. However, its role in autophagy in pancreatic cancer, one of the deadliest human malignancies, is unknown. Here, we investigated the function of YY1 in pancreatic cancer cells autophagy and its mechanisms of action. The activity of cells undergoing autophagy was assessed using transmission electron microscopy, immunofluorescence, and Western blotting. A luciferase activity assay, real-time quantitative polymerase chain reaction (RT-qPCR), and chromatin immunoprecipitation (ChIP) were also used to identify putative downstream targets of YY1. YY1 was confirmed to regulate autophagy in pancreatic cancer cells. It was found to directly regulate the expression of miR-30a, a known modulator of autophagy-associated genes. Furthermore, overexpression of miR-30a attenuated the pro-autophagic effects of YY1. Cumulatively, our data suggest that miR-30a acts in a feedback loop to modulate the pro-autophagic activities of YY1. Thus, autophagy in pancreatic cancer cells may be regulated, in part, by a tightly coordinated YY1/miR-30a regulatory circuit. These findings provide a potential druggable target for the development of treatments for pancreatic cancer.
ISSN:1479-5876
1479-5876
DOI:10.1186/s12967-017-1308-3