# The Clinical Role of SRSF1 Expression in Cancer: A Review of the Current Literature
## 3 Results
### Review
#### 3.2.1 Prostate

Table 1: Summary table. All the characteristics of the studies included, where reported. the synthesis of M and S HSD17B2 isoforms that do not suppress DHT synthesis, promoting cancer progression and development in vitro and in the xenograft model in vivo [20]. In 2020, [PERSON] et al. performed a WGS (Whole Genome Sequencing) and RNA sequencing on tissues collected from patients affected by mCRCP (Castration-Resistant Prostate Cancer), to investigate if any genomic changes occurred. Based on their response to chemotherapy, patients were divided into two groups: Enzalutamide-resistant and Enzalutamide-naive. The authors found that there was no statistical difference in copy gain events between the genomes of the two groups of patients; therefore, the most important differences were revelaed in the copy loss of genes. In particular, it was intriguing to find that the copy loss occurs in 17q22; this cytoband, in fact, is where SRSF1 and RNF43 genes are located. It is even more interesting to detect that the loss of these two genes was found in enzalutamide-resistant patients only. The authors then performed a survival analysis stratified by the deletion of SRSF1 and RNF43 and revealed that the deletion of 17q22 was related to poor prognosis and OS (overall survival). After they performed an MR (Master Regulator) analysis, an algorithm to predict variation in regulations related to a specific deletion, they identified that the loss of 17q22 containing SRSF1 and RNF43 could positively influence the activity of PLK1, AKT1 and cyclin-dependent kinases (CDK1 and CDK2) playing a well-known role in cell-cycle and tumorigenesis in prostate cancer [21]. In conclusion, the authors found a likely clinical role of SRSF1 and RNF43 in prostate cancer; resistance to enzalutamide therapy and reduction of OS. Our group published a paper in 2021 reporting the construction of TMA (tissue microarray) blocks with a semi-automatic tissue microarray, the Galileo TMA CK3500 (Integrated System Engineering, Milan, Italy). We analyzed the clinical data of 368 patients who had undergone surgery for PCa or BPH (Benign Prostate Hyperplasia) in a single institution and obtained samples of tissues from paraffin blocks to construct the TMA blocks; we than performed an IHC (immunohistochemistry) analysis, where pathologists did not know clinical data of patients. We evaluated the expression of multiple proteins and SRSF1, we also evaluated MVD (microvascular density), because previous studies revealed that SRSF1 could regulate the AS of VEGF (vascular endothelial growth factor) and its different activities and its role in cancer progression [8; 10], we then correlated histological features with clinical data. We found that SRSF1 and MVD were more expressed in patients with Pca than BPH and were also related to clinical features, in particular the expression of SRSF1, while high MVD was related both to worse OS and biochemical recurrence at 5 and 9 years in patients with Pca. SRSF-1+ patients had worse 5- and 9-year biochemical recurrence (36% and 6%) with respect to SRSF-1\(-\) (67% and 7%; \(p<0.01\)) and similarly MVD+ patients (44% and 7%) with respect to MVD\(-\) (64% and 8%; \(p<0.01\)). Restricting the analysis only to patients with PC and diabetes, we found that SRSF-1+ was associated with Ki-67+ (OR: 8.75; \(p<0.05\)) and MVD+ (OR: 7.5; \(p<0.05\)). Regarding histological features, SRSF1 was related to overall MVD and with positive Ki67, the expression of Androgen Receptor (AR), Insulin Receptors (IR), insulin-like growth factor 1-receptor (IGF1-R), and the expression of prostate specific membrane antigen (PSMA); MVD was related to the expression of SRSF1 and also with positive Ki67, expression of Insulin Receptors (IR), (insulin-like growth factor 1-receptor) IGF1-R, and the expression of prostate specific membrane antigen (PSMA). In the sub-cohort of patients affected with PCa, SRSF1 was also related to the expression of AR, Ki67, IR and MVD [22].