Siyuan Cheng

This study identifies INSM1 as a key regulator of neuroendocrine plasticity and tumor progression in prostate cancer, showing its role in lineage programs and identifying HHT as a potential therapeutic agent.

This study identifies March5 as a muscle proteostatic checkpoint that limits ATF4-dependent GDF15 production, linking muscle health to feeding and body composition.

The paper identifies RUNX1T1 as a marker of lineage plasticity across cancers and shows that targeting the RUNX1T1-HDAC complex can suppress plastic cell growth.

This study identifies Notch signaling as a graded rheostat regulating lineage plasticity and therapy resistance in prostate cancer, showing that intermediate Notch activity maintains stem-like progenitor states and that modulating Notch levels can restore drug sensitivity.

SCAPE provides an AI-driven platform for comprehensive single-cell data analysis, demonstrating its utility in lung cancer progression studies.

This study identifies Notch signaling as a driver of lineage plasticity and therapeutic resistance in enzalutamide-resistant prostate cancer and shows its inhibition reverses resistance in vitro.

This study identifies TET2 activation in slow-cycling cells as a driver of prostate cancer progression through epigenetic changes and shows targeting TET2 suppresses tumor growth.

This study investigates Wnt/beta-Catenin signaling in neuroendocrine prostate cancer, finding elevated pathway activity and potential therapeutic targeting.

This study investigates AR-driven gene expression and epigenetic changes in prostate cancer using multi-omics data from LNCaP cells, identifying gene expression shifts and AR binding patterns under androgen deprivation therapy.