AI Article Synopsis
- The study investigated how melatonin, found in certain edible plants, affects metastasis in colorectal cancer through its interaction with TMPRSS4 and EMT signaling in HCT15 and SW620 cancer cells.
- Melatonin showed limited cytotoxic effects but significantly reduced cancer cell invasiveness and migration, while altering the expression of various proteins related to metastasis.
- The results indicate that melatonin may inhibit metastasis in colon cancer by suppressing TMPRSS4-related processes, enhancing E-cadherin expression, and altering other key signaling pathways.
Article Abstract
In the current study, the underlying anti-metastatic mechanism of melatonin contained in some edible plants was explored in association with transmembrane protease serine 4 (TMPRSS4) mediated metastasis and epithelial-mesenchymal transition (EMT) signaling in human HCT15 and SW620 colorectal cancer cells. Here, TMPRSS4 was highly expressed in HCT15, but was weakly expressed in SW620 cells. Melatonin exerted weak cytotoxicity, decreased invasion, adhesion, and migration, and attenuated the expression of TMPRSS4, cyclin E, pro-urokinase-type plasminogen activator (pro-uPA), p-signal transducer and activator of transcription 3 (p-STAT3), p-focal adhesion kinase (p-FAK), Snail and increased the expression of E-cadherin, p27, pp38 and p-Jun N-terminal kinases (p-JNK) in HCT15 cells. Conversely, overexpression of TMPRSS4 reduced the ability of melatonin to activate E-cadherin and reduce Snail. Furthermore, even in SW620 cells transfected with TMPRSS4-overexpression plasmid, melatonin effectively suppressed invasion and migration along with decreased expression of Snail, cyclin A, cyclin E, pro-uPA and p-FAK and increased expression of E-cadherin and p27. Overall, these findings provide evidence that melatonin suppresses metastasis in colon cancer cells via inhibition of TMPRSS4 mediated EMT.
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| http://dx.doi.org/10.1002/ptr.7156 | DOI Listing |
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