LncRNA TP73‐AS1 enhances the malignant properties of pancreatic ductal adenocarcinoma by increasing MMP14 expression through miRNA ‐200a sponging

Pancreatic ductal adenocarcinoma (PDAC) is an invasive and aggressive cancer that remains a major threat to human health across the globe. Despite advances in cancer treatments and diagnosis, the prognosis of PDAC patients remains poor. New and more effective PDAC therapies are therefore urgently re...

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Bibliographic Details
Published in:Journal of cellular and molecular medicine 2021-04, Vol.25 (7), p.3654-3664
Main Authors: Miao, Haiyan, Lu, Jingjing, Guo, Yibing, Qiu, Hongquan, Zhang, Yu, Yao, Xihao, Li, Xiaohong, Lu, Yuhua
Format: Article
Language:English
Subjects:
Adenocarcinoma
Antibodies
Apoptosis
Cell culture
Cell cycle
Cell growth
Cell survival
ceRNA
Flow cytometry
Gene expression
Invasiveness
Laboratory animals
Liver cancer
Lymph nodes
Medical prognosis
Metastases
Metastasis
MicroRNAs
Microscopy
miRNA
miR‐200a
mmp14
Non-coding RNA
Pancreatic cancer
pancreatic ductal adenocarcinoma
Pheochromocytoma cells
Short Communication
Therapeutic targets
TP73‐AS1
Tumor cell lines
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Summary:Pancreatic ductal adenocarcinoma (PDAC) is an invasive and aggressive cancer that remains a major threat to human health across the globe. Despite advances in cancer treatments and diagnosis, the prognosis of PDAC patients remains poor. New and more effective PDAC therapies are therefore urgently required. In this study, we identified a novel host factor, namely the LncRNA TP73‐AS1, as overexpressed in PDAC tissues compared to adjacent healthy tissue samples. The overexpression of TP‐73‐AS1 was found to correlate with both PDAC stage and lymph node metastasis. To reveal its role in PDCA, we targeted TP73‐AS1 using LnRNA inhibitors in a range of pancreatic cancer (PC) cell lines. We found that the inhibition of TP73‐AS1 led to a loss of MMP14 expression in PC cells and significantly inhibited their migratory and invasive capacity. No effects of TP73‐AS1 on cell survival or proliferation were observed. Mechanistically, we found that TP73‐AS1 suppressed the expression of the known oncogenic miR‐200a. Taken together, these data highlight the prognostic potential of TP73‐AS1 for PC patients and highlight it as a potential anti‐PDAC therapeutic target.
ISSN:1582-1838
1582-4934
DOI:10.1111/jcmm.16425