ArticleOncology letters2020
Autophagy promotes malignant migration and invasion via miR-224-5p/BCL2 in pancreatic mucinous cystadenocarcinoma MCC1 cells.
Article in Oncology letters, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Autophagy Involvement in Non-Neoplastic and Neoplastic Endometrial Pathology: The State of the Art with a Focus on Carcinoma.International journal of molecular sciences · 2024Review
- Article
- Long non-coding RNA SNHG8 promotes autophagy as a ceRNA to upregulate ATG7 by sponging microRNA-588 in colorectal cancer.Oncology letters · 2021Article
- miR‑224‑5p regulates the proliferation, migration and invasion of pancreatic mucinous cystadenocarcinoma by targetingMolecular medicine reports · 2021Article
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The prognosis of invasive pancreatic mucinous cystadenocarcinoma (MCC) is poor, and the molecular mechanism underlying its development remains unclear. The present study aimed to explore the potential role of autophagy in pancreatic MCC. The results demonstrated an increase in autophagy signaling in pancreatic MCC tissues and the MCC1 cell line compared with adjacent tissues and normal human pancreatic ductal epithelium (HPDE) cells. In addition, abnormal autophagy activation facilitated the migration and invasion of MCC1 cells. MicroRNA (miR)-224-5p expression levels were significantly higher in MCC1 cells compared with those in HPDE cells. Treatment with rapamycin further demonstrated that high levels of autophagy elevated miR-224-5p expression in MCC1 cells in a time-dependent manner. BCL2 was identified as a downstream target gene of miR-224-5p, which binds to the 3'-untranslated region of BCL2. In addition, the results of the present study demonstrated that BCL2 knockdown reversed the inhibition of autophagy mediated by the miR-224-5p inhibitor. To the best of our knowledge, this is the first study to evaluate the role of autophagy in pancreatic MCC. Thus, these results suggested that autophagy may be hyperactivated in pancreatic MCC. In addition, the present study identified a positive feedback loop between autophagy signaling and miR-224-5p, which may promote the aggressive migration and invasion of MCC1. These results may provide a new insight into the relationship between autophagy and tumor metastasis in pancreatic MCC.
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