ID1 (Inhibitor Of DNA Binding 1, HLH Protein)

The METTL3-IGF2BP3 axis facilitates OS progression by enhancing ID1 mRNA stability and expression, highlighting its potential as a therapeutic target.

Encouragingly, significant strides have yielded promising antileukemic effects of ID1 inhibitors, both alone and in combination with targeted therapies against oncogenic signaling pathways. Nevertheless, further efforts are needed to develop innovative and practical strategies that modulate ID1 activity to restore and sustain hematopoietic homeostasis.

Furthermore, overexpression of ID1 promoted the progression of esophageal cancer, and the expression of ID1 in human cancerous tissues was significantly higher than that in peritumoral tissues. ID1 promotes the progression of esophageal cancer by inducing proliferation and immune suppression through regulation of the PTEN/YAP/Galectin-3 signaling pathway.

Our findings demonstrate that hypoxia drives pancreatic tumor progression by downregulating TRIM21, leading to stabilization of the oncogenic protein ID1. The TRIM21-ID1 axis emerges as a promising therapeutic target for PAAD, suggesting that restoring TRIM21-mediated ID1 degradation could counteract hypoxia-induced malignancy.

Mechanistically, p16 expression, senescence, and apoptosis were increased, and proliferation decreased in Tet2-/-;Id1-/- HSPCs. Thus, ID1 may represent a therapeutic target to reduce CH and delay the onset of disease.

Intriguingly, disrupting CREB5 super-enhancers with ABBV-075 significantly reduces its expression and inhibits H3.3K27M DIPG tumor growth. Combined treatment with ABBV-075 and a BRG1 inhibitor presents a promising therapeutic strategy for clinical translation in H3.3K27M DIPG treatment.

Additionally, Id1 knockdown in 4T1.13 murine breast cancer cells demonstrated reduced tumour growth and metastasis in vivo. Taken together, this study further implicates ID1 in a vascular program within cancer cells that supports disease progression.

Finally, PSAT1 promoted CRC proliferation by negatively regulating AMOT in vivo. PSAT1 could enhance the progression of colorectal cancer by regulating Hippo-YAP/TAZ-ID1 axis via AMOT, which is independent of the metabolic function of PSAT1.

TAM promotes CCA progression and chemoresistance through activating OSM-Yap-ID1.

Low expression of GREM2 in breast cancer cells is associated with hypermethylation of the GREM2 promoter, which may ultimately contribute to poor patient survival. GREM2 participates in regulating the expression of various genes, including ID1, and is involved in suppressing the proliferation of breast cancer cells. This suggests that GREM2 has the potential to act as a novel tumor suppressor in breast cancer.

This work reveals a surprising field effect of melanoma initiation in vivo in which tumors arise from within a zone of morphologically distinct, but clinically covert, precursors with altered transcriptional fate. Our studies identify novel targets that could improve early diagnosis and prevention of melanoma.

Because of the regulation function of the ID family in many processes, the up or down regulation of IDs genes in tumors Proves how important its tumor development, and therefore those proteins can be used as an indicator for CRC.