SYNCRIP (Synaptotagmin Binding Cytoplasmic RNA Interacting Protein)

Incorporating insights from spatial transcriptomics and single-cell analysis, this review provides a mechanistic foundation for the development of exosome-centered, redox-modulating therapeutics. Ultimately, this work aims to guide future research and drug discovery efforts toward integrating herbal medicine and redox biology in the fight against cancer.

The PPI network identified 11 hub genes with the strongest interactions with ELAVL1. These findings indicate that SG-related genes (DNAJA1, ELAVL1, FBL, GRB7, MOV10, PABPC3, PCBP2, PFN1, RFC4, SYNCRIP, USP10, ZFP36, and ZFP36L1) can be used to predict OC prognosis.

SYNCRIP is upregulated in CRC, and highly expressed SYNCRIP can accelerate CRC cell division by exerting its epigenetic regulatory effects. In addition, SYNCRIP is expected to become a potential biomarker to predict the effect of radiotherapy.

Our study provides a preliminary understanding of YBX1 PPI and the potential of flavonoids to disrupt these interactions. This study investigates the potential of flavonoids to target YBX1 PPIs, providing insights into novel therapeutic strategies for YBX1-driven cancers.

Exosomal miR-127-3p further stimulates M1 polarization of macrophages by suppressing ZC3H4. Taken together, the detailed understanding of the mechanisms through which β-elemene induces autophagy in NSCLCs and facilitates M1 polarization of macrophages provides compelling scientific evidence supporting its potential utility in NSCLC treatment.

More importantly, our in vivo experiments showed that SYNCRIP depletion significantly inhibited colorectal tumor growth. Taken all together, our results suggest SYNCRIP as a potent therapeutic target in colorectal cancer.

This observation is consistent with the survival curve for liver cancer patients from the TCGA database, which indicates that high expression of hnRNP Q is a prognostic marker for a poor outcome in individuals afflicted with hepatocellular carcinoma. Together, our findings suggest that hnRNP Q interacts with LIN28B and modulates the LIN28B/let-7 axis in hepatocellular carcinoma.

Here, using ex vivo paired ovarian cancer ascites obtained before and after chemotherapy and in vitro therapy-induced secretomes, we show that molecules secreted by ovarian cancer cells upon therapy promote cisplatin resistance and enhance DNA damage repair in recipient cancer cells...Thus, SNU13 and SYNCRIP spliceosomal proteins promote therapy resistance, while the exogenous U12 and U6atac snRNAs stimulate tumor growth. These findings demonstrate the significance of spliceosomal network perturbation during therapy and further highlight that extracellular signaling might be a key factor contributing to the emergence of ovarian cancer therapy resistance.

The above-mentioned genes can be used as diagnostic and therapeutic serum markers of transplantation rejection in renal patients. The newly predicted biomarkers and pathways require further studies.