SNCG (Synuclein Gamma)

SNCG and BCL6 demonstrate strong potential as dual non-invasive biomarkers for early endometriosis detection, particularly in menstrual fluid. Their combined use enhances diagnostic accuracy, offering a promising alternative to invasive methods. Further validation is needed to advance clinical translation and address urgent needs for timely diagnosis.

SNCG drives Bev resistance in CRC by forming a ternary complex with VEGF and VEGFR2, enhancing VEGFR2 signaling and angiogenesis. Dual targeting of VEGF and SNCG represents a promising therapeutic strategy to overcome Bev resistance, with the potential to improve outcomes in CRC patients.

Overall, our findings elucidated that miR-107 attenuated migration and EMT in OSCC by targeting SNCG and inhibiting the ERK1/2/NF-κB pathway, providing novel potential therapeutic targets for OSCC.

Additionally, the levels of the phosphorylated forms of FAK, AKT, and mTOR were significantly reduced in both AGS/DDP and SGC-7901/DDP cells treated with the combination of DDP and SSD, whereas the PTEN expression level increased. Our findings highlight the importance of alternative components within the tumor microenvironment for GC therapy and identify FAK/AKT/mTOR signaling as a potential target of SSD, providing novel insights into the mechanism by which SSD improves DDP resistance in GC.

P=N/A, N=360, Completed, Gynecologic Oncology Group | Not yet recruiting --> Completed

Subsequent experiments with STAT5b interference and ERK1/2 inhibitor treatment reversed the effects of SNCG on OSCC cell proliferation, apoptosis and cell cycle progression. Our findings suggest that SNCG functions as an oncogene in OSCC by targeting the JAK2/STAT5b axis and thus may be a potential new prognostic marker and therapeutic target in OSCC.

The results demonstrate that SGJY may inhibit the growth of breast cancer. The mechanism might involve downregulating the level of serum estradiol, and suppressing the protein expression in the SNCG/ER-α/AKT-ERK pathway.

Methods We performed scRNA-seq of pre-and post-treatment EUS-FNB biopsies and blood from 18 PDAC patients receiving Abraxane plus gemcitabine chemotherapy (AG). Conclusions Advanced PDAC patients with a high proportion of SNCG + tumor cells, SPP1 + macrophages Tex at baseline may indicate an ineffective AG chemotherapy. Moreover, this work highlights tumor conversion and interaction with TIME as major determinants of chemotherapy outcomes and identifies targeting CD276, a key driver of the tumor state, as a potential strategy to reverse chemo-resistance in PDAC.