Knockdown of TRIM44 inhibits the proliferation and invasion in prostate cancer cells
Oncology Research, ISSN: 1555-3906, Vol: 25, Issue: 8, Page: 1253-1259
2017
- 33Citations
- 5Captures
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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
- Citations33
- Citation Indexes33
- 33
- CrossRef26
- Captures5
- Readers5
Article Description
Tripartite motif 44 (TRIM44), a member of the TRIM protein family, has been shown to play a role in tumor development and progression. However, the potential involvement of TRIM44 in prostate cancer has not been fully explored. Therefore, in the present study, we analyzed the expression of TRIM44 in prostate cancer and assessed the role of TRIM44 in the progression of prostate cancer. Our results showed that the expression of TRIM44 was significantly upregulated in human prostate cancer cell lines. In addition, knockdown of TRIM44 significantly inhibited the proliferation, migration, and invasion of prostate cancer cells in vitro, as well as attenuated the tumor growth in vivo. Mechanistic studies showed that knockdown of TRIM44 significantly reduced the levels of phosphorylated PI3K and Akt in PC-3 cells. In conclusion, this study provided evidence that knockdown of TRIM44 inhibited proliferation and invasion in prostate cancer cells, at least in part, through the inactivation of the PI3K/Akt signaling pathway. These results suggest that TRIM44 may be a potential therapeutic target for the treatment of prostate cancer.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85029153294&origin=inward; http://dx.doi.org/10.3727/096504017x14854310794561; http://www.ncbi.nlm.nih.gov/pubmed/28160462; http://www.ingentaconnect.com/content/10.3727/096504017X14854310794561; http://www.ingentaconnect.com/content/cog/or/2017/00000025/00000008/art00005; https://www.techscience.com/or/v25n8/56910
Cognizant, LLC
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