Krüppel-like factor 4 (KLF4) is a member of the KLF transcription factor family containing zinc-fingers, and is involved in the regulation of apoptosis, proliferation and differentiation of B cells and B-cell malignancies. KLF4 can act like an oncogene, we shown that KLF4 overexpression correlated with poor prognostic and chemoresistance in B-NHL. In addition, we shown that KLF4 is regulated by YY1. In this study, we demonstrate that chemical inhibition of KLF4 by Kenpaullone, results in suppression of proliferation, cell survival, downregulation of Bcl-2 and increases apoptosis in B-NHL cell lines through YY1 independent pathway. Combination of Kenpaullone and Doxorubicin, increased apoptosis. The co-expressions of KLF4/YY1 or KLF4/Bcl-2 in NHL was analyzed using Oncomine Database, exhibiting a positive correlation of expression. The present findings suggest that the chemical inhibition of KLF4 by Kenpaullone treatment could be a potential therapeutic alternatively in KLF4 lymphomas.
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http://dx.doi.org/10.1080/10428194.2020.1869960 | DOI Listing |
Dev Cell
December 2024
Developmental Biology Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA; Biochemistry, Cell and Molecular Biology Program, Weill Cornell Graduate School of Medical Sciences, New York, NY 10021, USA. Electronic address:
Two distinct lineages, pluripotent epiblast (EPI) and primitive (extra-embryonic) endoderm (PrE), arise from common inner cell mass (ICM) progenitors in mammalian embryos. To study how these sister identities are forged, we leveraged mouse embryonic stem (ES) cells and extra-embryonic endoderm (XEN) stem cells-in vitro counterparts of the EPI and PrE. Bidirectional reprogramming between ES and XEN coupled with single-cell RNA and ATAC-seq analyses showed distinct rates, efficiencies, and trajectories of state conversions, identifying drivers and roadblocks of reciprocal conversions.
View Article and Find Full Text PDFVavilovskii Zhurnal Genet Selektsii
November 2024
Institute of Cytology and Genetics of the Siberian Branch of the Russian Academy of Sciences, Novosibirsk, Russia Institute of Chemical Biology and Fundamental Medicine of the Siberian Branch of the Russian Academy of Sciences, Novosibirsk, Russia.
Frontotemporal dementia with parkinsonism-17 is a neurodegenerative disease characterised by pathological aggregation of the tau protein with the formation of neurofibrillary tangles and subsequent neuronal death. The inherited form of frontotemporal dementia can be caused by mutations in several genes, including the MAPT gene on chromosome 17, which encodes the tau protein. As there are currently no medically approved treatments for frontotemporal dementia, there is an urgent need for research using in vitro cell models to understand the molecular genetic mechanisms that lead to the development of the disease, to identify targets for therapeutic intervention and to test potential drugs to prevent neuronal death.
View Article and Find Full Text PDFJ Biochem Mol Toxicol
January 2025
Anqing Medical College Clinical Research Center, Anqing Municipal Hospital, Anqing, Anhui, P.R. China.
Our previous research identified that lncRNA PVT1 is upregulated in patients with IA. However, the precise functions of PVT1 in IA remain unclear. We compared the levels of PVT1, caspase-3, caspase-1, and NLRP3 in normal and IA patients.
View Article and Find Full Text PDFWorld J Methodol
December 2024
Department of Biology, St. Francis College, Brooklyn, NY 11201, United States.
In this Editorial review, we would like to focus on a very recent discovery showing the global autosomal gene regulation by Y- and inactivated X-chromosomal transcription factors, zinc finger gene on the Y chromosome (ZFY) and zinc finger protein X-linked (ZFX). ZFX and ZFY are both zinc-finger proteins that encode general transcription factors abundant in hematopoietic and embryonic stem cells. Although both proteins are homologs, interestingly, the regulation of self-renewal by these transcriptional factors is almost exclusive to ZFX.
View Article and Find Full Text PDFAm J Physiol Renal Physiol
December 2024
Division of Nephrology, Department of Medicine, Stony Brook University, , Stony Brook, NY.
Glomerular endothelial cell (GEnC) injury is a common feature across the wide spectrum of glomerular diseases. We recently reported that the endothelial-specific knockout of increases the susceptibility to GEnC injury and subsequent development of subacute thrombotic microangiopathy (TMA). However, the mechanism(s) mediating GEnCs response to injury in TMA are poorly understood.
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