ACTL6A depletion induces KLF4-mediated anti-tumorigenic effects in colorectal cancer
8.0
来源：
Nature
发布时间：
2025-08-28 19:35
摘要：
ACTL6A is identified as a pivotal epigenetic regulator in colorectal cancer (CRC), where its depletion leads to enhanced KLF4-mediated transcriptional activation of tumor-suppressive genes, promoting apoptosis and inhibiting cell proliferation. The study employs integrated multi-omics approaches to demonstrate that ACTL6A regulates chromatin accessibility and gene expression, highlighting its potential as a therapeutic target in CRC. The findings suggest that targeting ACTL6A could reactivate silenced tumor-suppressive gene networks, offering new avenues for CRC treatment.
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关键证据
ACTL6A depletion significantly reduced cell viability and induced apoptosis.
The study shows that ACTL6A regulates chromatin accessibility and gene expression in CRC.
Targeting ACTL6A may serve as a promising therapeutic strategy in CRC.
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AI评分总结
ACTL6A is identified as a pivotal epigenetic regulator in colorectal cancer (CRC), where its depletion leads to enhanced KLF4-mediated transcriptional activation of tumor-suppressive genes, promoting apoptosis and inhibiting cell proliferation. The study employs integrated multi-omics approaches to demonstrate that ACTL6A regulates chromatin accessibility and gene expression, highlighting its potential as a therapeutic target in CRC. The findings suggest that targeting ACTL6A could reactivate silenced tumor-suppressive gene networks, offering new avenues for CRC treatment.