It is established that HBZ inhibits hnRNPA1 transcription, therefore allowing HTLV-1 to hijack host RNA splicing and to generate an oncogenic isoform that drives transformation and chemoresistance and position HBZ splicing and its regulators as therapeutic targets in ATL.
PTBP1 is established as a critical regulator of AML cell fitness and a clinically actionable therapeutic combination that exploits AML dependency on PTBP1-CDC42 signaling to enhance the efficacy of venetoclax-based regimens is identified.
A specific protein (SRSF2) acts like a rogue editor, altering the genetic instructions of another molecule (hnRNPD) and creates a “shield” (PD-L1) on the surface of the cancer cell, effectively blinding the immune system and allowing the tumor to grow unchecked.
Zhao Cheng, Lin Jiang, Ming-yang Wang et al.· Oncogene· 0 citations
The authors' computational framework proposes that the HNRNPD-MAP4K4 splicing axis links apoptotic dysregulation to immune microenvironment remodeling in Wilms’ tumor.
Chun-chun Yang, Man Liao, Haolun Xu et al.· PLoS ONE· 0 citations
A novel TRDMT1-TFRC regulatory axis that suppresses LUAD progression through the modulation of ferroptosis is unveiled, highlighting this pathway as a promising therapeutic target for future interventions.
Ying Zhu, Zu-Li Jiang, You-Ming Chen et al.· Journal of Biological Chemis...· 0 citations
EIF4A3-dependent NMD is defined as a checkpoint linking RNA surveillance to oncogenic fusion-isoform dosage, leukemic fitness, and chemosensitivity in t(8;21) AML, providing a mechanistic explanation for clinical heterogeneity in t(8;21) AML.
Min Zhang, Yisheng Li, Bin Zhang et al.· Leukemia· 1 citation
Initial evidence for a novel role of FOXP3 as a tumor suppressor in T-ALL through modulation of TAL1 transcriptional activity is provided through modulation of TAL1 transcriptional activity.
V. Fleskens, M. Mokry, A. M. van der Leun et al.· 0 citations
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