AI Article Synopsis
- Mantle cell lymphoma (MCL) is an aggressive form of non-Hodgkin lymphoma with a poor prognosis, and Krüppel-like factor 4 (KLF4) is implicated in its progression.
- KLF4 is downregulated in MCL cell lines and patient lymph nodes, which correlates with a worse prognosis; its regulation can inhibit cell growth and promote apoptosis in specific MCL cells.
- Researchers found that the KLF4 protein interacts with β-catenin and can suppress key oncogenes, suggesting that boosting KLF4 levels might be a potential therapeutic strategy, possibly through the use of DNMT-1 inhibitors like 5-azacytidine to restore its expression.
Article Abstract
Mantle cell lymphoma (MCL) is an aggressive subtype of B-cell non-Hodgkin lymphoma (NHL) with poor prognosis. Krüppel-like factor 4 (KLF4) has been reported as a bi-regulator in malignancies, but little is known about its role in MCL. Here, we showed that KLF4 was downregulated in three MCL cell lines and lymph nodes from MCL patients, which resulted in a negative prognosis. We also found that the regulation of KLF4 could inhibit the proliferation and induce apoptosis of Jeko-1 cells. The lentivirally over-expressed KLF4 protein was found bind to β-catenin and could inhibit downstream molecules such as cyclinD1 and c-Myc. Furthermore, 5-azacytidine could decrease the expression of methyltransferase-1 (DNMT-1) and restore the KLF4 expression in MCL cell lines, indicating that methylation might play an important role in the downregulation of KLF4. KLF4 may be a potential therapeutic target as a tumor suppressor in MCL.
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| http://dx.doi.org/10.1080/10428194.2017.1292354 | DOI Listing |
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