ABSTRACT
This study aimed to examine the potential role of STK15 in Heptaocellular tumohgenesis. We analyzed the STK15 [protein and mRNA] expression and try to correlate STK15 expression with chromosome ploidy, various clinicopathological and molecular features of HCC. We aimed to evaluate chromosomal instability [CIN] by evaluating chromosome ploidy analyses, and correlate polsomy with various molecular features of HCC. Primary histologically proved HCC and adjacent nontumorous liver tissues from 29 patients were selected and surgically resected from Tanta University Hospital and Menophyia University Hospital. The tumor tissue and paired adjacent noncancerous liver tissue were obtained independently. We analyzedjhe STK15 expression by evaluating its mRNA and protein expression status using RT-PCR and Western blot and analysis. We try to correlate STK15 expression with chromosomae ploidy, various clinicopathological and molecular features. For chromosome ploidy analyses, FISH was carried out with direct fluorescence-labeled -satellite probes for chromosome 3,7,17 and 18 in both HCC and in adjacent noncancerous liver tissue. In the present study we demonstrated overexpression of STK15 protein in HCC. STK15 protein expression was highly elevated in 20 of the 29 tumors [69%] examined with 8 tumors displaying a >10-fold increase. It appeared that the extent of STK 15 protein expression, was more frequently associated with high grade and higher siage of the tumors. STK 15 mRNA was overexpressed in 20 tumors [69%]. In the nontumorous liver, STK15 mRNA was overexpressed in 2 cases [7%]. STK15 overexpression in HOC did not correlate with age, gender chronic HCV infection, and chronic HBV infection, but was associated with serum -fetoprotein elevation [P = 0.04]. Histologically, STK15-mRNA overexpression was more frequent in grade II-IIIB [P = 0.006]. STK15-mRNA overexpression was associated with portal vein tumor invasion [stage 1 1 IB HCC; P = 0.033], regardless of tumor size. As regard chromosomal ploidy all examined chromosomes were found to be aneuploid to a similar extent. The modal copy number of each chromosome ranged from two copies [disomy] to six copies [hexasomy], and the percentage of cells that did not carry the modal copy number was quite variable. Nine tumors [31%] showing numerical heterogeneity in all four examined chromosomes, were judged to be carrying CIN. Possible associations between the presence of CIN and potential prognostic factors [gender, age, tumor size, tumor stage, and differentiation grade] were examined by the X2 test, and none were identified. In summary, we have demonstrated that STK15 is highly expressed in HCC. Overexpression of STK15 may have important pathogenetic and prognostic significance in HCC. Also we can conclude that, CIN can be detectable in primary HCC using FISH technique. The STK15/BTAK/Aurora. A pathway play roles in hepatocellualr carcinogenesis and, therefore, could prove to be relevant novel disease markers and therapeutic targets