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Zhan-Cheng Zeng

Researcher at Sun Yat-sen University

Publications -  15
Citations -  401

Zhan-Cheng Zeng is an academic researcher from Sun Yat-sen University. The author has contributed to research in topics: Leukemia & DOT1L. The author has an hindex of 4, co-authored 11 publications receiving 131 citations.

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CircMYBL2, a circRNA from MYBL2, Regulates FLT3 Translation by Recruiting PTBP1 to Promote FLT3-ITD AML Progression

TL;DR: This work is the first to reveal a circRNA that specifically influences FLT3-ITD AML and regulatesFLT3 kinase levels through translational regulation, suggesting that circMYBL2 may be a potential therapeutic target for F LT 3-ITd AML.
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N6-methyladenosine methyltransferases: functions, regulation, and clinical potential

TL;DR: In this article, the authors summarize the function of these m6A methyltransferases or complexes in regulating the key genes and pathways of cancer biology and highlight the progress in the use of m6As in mediating therapy resistance, including chemotherapy, targeted therapy, immunotherapy and radiotherapy.
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circRNA circAF4 functions as an oncogene to regulate MLL-AF4 fusion protein expression and inhibit MLL leukemia progression.

TL;DR: It is shown that circAF4 plays an oncogenic role in MLL-AF4 leukemia and promotes leukemogenesis in vitro and in vivo, and a number of circRNAs could originate from these partners, suggesting the potential roles of fusion gene partner-originating circ RNAs in leukemia with chromosomal translocations.
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The lncRNA LAMP5-AS1 drives leukemia cell stemness by directly modulating DOT1L methyltransferase activity in MLL leukemia.

TL;DR: It is discovered that a long noncoding RNA (lncRNA) LAMP5-AS1 can promote higher degrees of H3K79 methylation, followed by upregulated expression of the self-renewal genes in the HOXA cluster, which are responsible for leukemia stemness in context of MLL rearrangements.
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Activation of the Lysosome-Associated Membrane Protein LAMP5 by DOT1L Serves as a Bodyguard for MLL Fusion Oncoproteins to Evade Degradation in Leukemia

TL;DR: This study demonstrates that LAMP5 serves as a “bodyguard” for MLL fusions to evade degradation and is the first to link H3K79 methylation to autophagy regulation, highlighting the potential of LAMP 5 as a therapeutic target for Mll leukemia.