Piezo1 act as a potential oncogene in pancreatic cancer progression
Life Sciences, ISSN: 0024-3205, Vol: 310, Page: 121035
2022
- 7Citations
- 12Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations7
- Citation Indexes7
- CrossRef5
- Captures12
- Readers12
- 12
Article Description
Pancreatic ductal adenocarcinoma (PDAC) is the fourth leading cause of cancer related death. A growing number of studies believe that matrix stiffness plays an important role in the development of pancreatic disease. As one of the famous mechanically activated cation channels, Piezo1 has received more attention recently. Here we tried to describe the role of Piezo1 on PDAC progression. It seemed that Piezo1 was a potential tumor-promoting marker of pancreatic cancer. By using Yoda1, we measured the intracellular calcium flux mediated by Piezo1 which confirmed it did act as an intrinsic cation channel in pancreatic cancer cells. Additionally, we also found the inhibition of Piezo1 could inhibit cancer progression in vitro ; however, Piezo1 activation (induced by Yoda1) had an oppositive effect. Moreover, Piezo1 activation may also accelerate pancreatic cancer tumor growth/formation via modulating pancreatic cancer cell-tumor microenvironment interactions in vivo. We concluded that Piezo1 acted as an oncogenic gene in pancreatic cancer progression. It might be one of promising targets for pancreatic cancer therapy.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0024320522007354; http://dx.doi.org/10.1016/j.lfs.2022.121035; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85139721577&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/36208662; https://linkinghub.elsevier.com/retrieve/pii/S0024320522007354; https://dx.doi.org/10.1016/j.lfs.2022.121035
Elsevier BV
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