SOS1 (SOS Ras/Rac Guanine Nucleotide Exchange Factor 1)

In xenograft models, CEBPB activates ERK1/2 via SOS1 upregulation, which subsequently promotes tumor growth and suppresses apoptosis (p < 0.01). CEBPB regulates ERK1/2 activity through SOS1 and contributes to OC progression.

This study identifies a novel mutation in the known HGF-related gene SOS1, which may potentially contribute to gingival overgrowth by disrupting the interaction between SOS1 and Grb2.

These findings demonstrate that DLEU2 facilitates BC progression via the miR-103a-2-5p/SOS1 axis. This study reveals a novel regulatory mechanism underlying BC development and highlights DLEU2 as a potential therapeutic target for BC treatment.

Herein, we report the discovery and initial optimization of a selective quinazoline-based compound series that binds with micromolar affinity to the catalytic site of SOS2. We also disclose an additional, previously unreported binding site on SOS2 occupied by a different small molecule class.

In this study, we described rare clinical manifestations and detected three novel variants in NF1, BRAF, and RIT1 genes. We propose that NGS technology enables the detection of variants in rare genes responsible for the etiology of RASopathies. The study, therefore, not only contributes to the existing literature but also expands the spectrum of genotype and phenotype of RASopathies.

Here, we investigated ERP29 impact on PSCC progression in cisplatin (CDDP)-sensitive (FaDu and LAU-2063), CDDP-treated (FaDu-CDDP), and CDDP-resistant (FaDu-R) cells...Lower ERP29 and higher miR-4421 expressions were predictive of poor survival, suggesting a potential therapeutic use for miR-4421 inhibitors. Upon validation, these findings may contribute to targeted therapies for PSCC based on ensuring ERP29 expression.

Following local IR exposure, serum exosomes cross the BBB to promote the progression of distant gliomas. Exosomal microRNAs play an important role in this process.

Furthermore, PPVII exerted strong antitumor effects in vivo in nude mice injected with breast cancer cells. Our results suggest that PPVII may promote apoptosis through regulating the SOS1/MAPK/ERK pathway, making it a possible candidate target for the treatment of breast cancer.

This study reveals a novel mechanism underpinning self-renewal and tumor growth of CSLC (cancer stem cell) in NSCLC and identifies potential therapeutic targets for NSCLC treatment.

The confocal laser microscopy examination shows PW06 increased E-cadherin but decreased vimentin in MIA PaCa-2 cells. Together, our findings strongly suggest that PW06 inhibited the p-Akt/mTOR/NF-κB/MMPs pathways, increased E-cadherin, and decreased N-cadherin/vimentin, suppressing the migration and invasion in MIA PaCa-2 cells in vitro.

ZNF513 combined with KIF3C regulates gingival fibroblast proliferation, migration, and fibrosis response via the PI3K/AKT/mTOR and Ras/Raf/MEK/ERK pathways. In summary, these results demonstrate ZNF513 + KIF3C as an important genetic combination in HGF manifestation and suggest that ZNF513 mutation may be a major risk factor for HGF.

Finally, we showed that GTP-bound RAS level underwent rebound even in BI3406-sensitive PDOs with no change of KRAS downstream effector genes, thus suggesting upregulation of guanine nucleotide exchange factor as potential cellular adaptation mechanisms to SOS1 inhibition. Taken together, our results show that high SOS1/SOS2 protein expression ratio predicts sensitivity to SOS1 inhibition and support further clinical development of SOS1-targeting agents in CRC.