Extend your brand profile by curating daily news.

Breakthrough Discovery: Key Protein Interaction Offers New Hope for Acute Myeloid Leukemia Treatment

By FisherVista

TL;DR

Identified mechanism in AML treatment offers strategic advantage by targeting JMJD1C-RUNX1 axis, potentially overcoming disease heterogeneity.

JMJD1C forms liquid-like condensates with RUNX1, activating key genes for AML cell survival by regulating gene expression.

Research on JMJD1C's role in AML presents new therapeutic strategy, aiming to improve patient outcomes and tackle disease heterogeneity.

Study reveals JMJD1C's unique function in leukemia biology by forming condensates, shedding light on potential new treatments for AML.

Found this article helpful?

Share it with your network and spread the knowledge!

Breakthrough Discovery: Key Protein Interaction Offers New Hope for Acute Myeloid Leukemia Treatment

Scientists from Tsinghua University and The Rockefeller University have revealed a groundbreaking mechanism for potentially treating acute myeloid leukemia (AML) by targeting the interaction between two key proteins, JMJD1C and RUNX1. The research, published in Protein & Cell, demonstrates how understanding this molecular interaction could provide a universal strategy for combating this aggressive and complex cancer.

AML is characterized by uncontrolled growth of immature blood cells, presenting significant challenges for treatment due to its genetic complexity. Traditional therapies often struggle to address the underlying transcriptional networks that sustain leukemic cells, making this discovery particularly significant. The study reveals that JMJD1C forms liquid-like molecular condensates when recruited by RUNX1 to specific genomic locations, activating genes crucial for leukemia cell survival and proliferation.

The researchers found that JMJD1C's non-catalytic functions, specifically its ability to form molecular condensates through its intrinsically disordered N-terminal region, are critical to leukemia cell maintenance. By disrupting JMJD1C's N-terminal region, researchers observed reduced leukemia cell viability, suggesting a potential therapeutic approach.

Dr. Mo Chen, a senior author of the study, emphasized the transformative potential of these findings, noting that the research uncovers a previously unknown role for JMJD1C in leukemia biology. The discovery offers hope for developing treatments that could work across multiple AML subtypes, addressing the disease's notorious heterogeneity.

This research represents a significant step forward in understanding and potentially treating AML. By targeting the JMJD1C-RUNX1 interaction, scientists may be able to disrupt the transcriptional programs that sustain leukemia cells, potentially offering a more universal approach to treatment. Future research will focus on translating these molecular insights into clinical interventions, potentially opening new pathways for leukemia treatment.

Curated from 24-7 Press Release

blockchain registration record for this content
FisherVista

FisherVista

@fishervista