SRI (Sorcin, 22 KDa Protein)

Sorcin was found to be higher in PCa compared to healthy males. In addition, high International Society of Urological Pathology grade groups were observed in patients with high sorcin levels.

High ERK1/2, Sorcin, and low Bcl2 expression prevailed in SRCC cases. These expressions were upregulated post-NACT in both subtypes. SRCC patients had shorter OS, moreover expression of ERK1/2, Sorcin, and Bcl2 correlated with poor survival outcomes and major clinicopathological factors in SRCC cases.

In this study, we revealed the mechanism of action of sorcin, which is a druggable target for inducing ferroptosis, we identified celastrol as a novel agent that induces ferroptosis, and we showed that disrupting the sorcin-PAX5 interaction is a promising therapeutic strategy for treating pancreatic cancer.

Its involvement in drug-resistant cancers further advert Sorcin as a promising therapeutic target. This review summarizes the mechanistic role of Sorcin in cancer, its contribution to drug resistance, clinical relevance, and the current and emerging therapeutic approaches aimed at translating Sorcin-targeted therapies into clinical practice.

Furthermore, plasma serpin E1 levels are higher in peripheral blood samples from PCAND patients than in those from T2DM patients. In conclusion, sorcin may be the key driver in PCAND, and further study on the sorcin-STAT3-serpin E1/CCL5 signaling axis may help us better understand the pathogenesis of PCAND and identify potential biomarkers.

Sorcin participates in several mechanisms of MDR, including drug efflux, drug sequestering, cell death inhibition, gene amplification, epithelial-to-mesenchymal transition, angiogenesis, and metastasis. The present review focuses on the structure and function of sorcin, on sorcin's role in cancer and drug resistance, and on the approaches aimed at targeting sorcin.

Mechanistically, SRI interacts with STAT3 and then activates the NF-κB signaling pathway in vitro and in vivo. SRI interacting with STAT3 inhibits apoptosis by the NF-κB pathway and further contributes to the proliferation in HCC, which offers a novel clue and a new potential therapeutic target for HCC.

Mechanistically, SRI regulated vascular endothelial growth factor A (VEGFA) and vascular endothelial growth factor B (VEGFB) through PI3K/Akt/FOXO1 signal pathway. Overall, our study indicates that SRI stimulates HCC growth by controlling VEGFA/B, which presents a fresh insight into the pathogenesis of hepatocarcinogenesis and a new therapeutic target for HCC.

Similarly, suppression of Caspase-1 reversed the inhibitory effect of Sorcin knockdown on the malignant progression of HCC via knockdown of Caspase-1 or the inhibitor VX765...Collectively, high Sorcin expression in HCC negatively regulates pyroptosis by interacting with the NLRP3 inflammasome to promote HCC proliferation, migration, and invasion. The results of this study provide a scientific basis for Sorcin as a new biomarker and potential therapeutic target for HCC.

Post-NACT group treated with 5-fluorouracil (2,600 mg/m2 as a 24 hr infusion), leucovorin (200 mg/ m2), oxaliplatin (85 mg/ m2), and docetaxel (60 mg/ m2), all given on the same day and administered every 2 weeks before surgery. Sorcin levels remain moderate to high in non-responders. Further, post-NACT group treated with FLOT identified to enhance the sorcin expression among the non-responders. Therefore, sorcin can be a potential biomarker to diagnose the multidrug resistance phenotype in advanced gastric cancer patients.