| Part 1:Clinical Analysis of Prostate Diseases in the ElderlyObjective: To investigate the clinical characteristics and relationship of the common prostate diseases in elderly people.Methods:Collected clinical datas of patients diagnosed with benign prostatic hyperplasia (BPH), prostate intraepithelial neoplasia (PIN) and prostate cancer (PCa). And all the patients were above the age of 60 years old. Midstream urine was cultured and serum prostate specific antigen(PSA) was detected using chemical luminescence assay.Results:The amount of prostate diseases in elderly people involved were 255 cases, including 111 cases of BPH,57 cases of PIN and 87 cases of PCa. The average ages in group BPH, PIN and PCa were 70.04±6.26,70.91±6.69,71.89±6.84 and there was no significant difference among these groups (P>0.05). Dysuria and urinary irritation symptoms were the main clinical symptoms in all these groups, while PCa patients could also suffer fever and bone pain related to tumor metastasis. Laboratory tests showed that the urine culture positive rates for BPH,PIN and PCa were 18.92%, 19.30% and 14.94% respectively, but there was no significant difference (P>0.05). The level of PSA in these group showed a increasing trend and it was significantly higher in patients with PCa than those with BPH and PIN (P<0.01).Conclusions:The average age, urine culture positive rate and the main clinical symptoms have no significant difference among elderly people diagnosed with BPH, PIN and PCa. While bone pain and remarkably increased PSA level are unique to PCa.Part 2: Effects of Calcium/Calmodulin Dependent Protein Kinase ? on Proliferation, Invasion and NF-?B/Snail/RKIP Signaling Pathway in Prostate Cancer CellsObjective: To investigate the effects of inactive calcium/calmodulin dependent protein kinase ?(CaMK?) on proliferation, invasion and NF-?B/Snail/RKIP signaling pathway related to epithelia-mesenchymal transition (EMT) in prostate cancer PC3 cells.Methods:KN93, a specific inhibitor of CaMK ? was used to suppress the activity of CaMK?in PC3 cells. MTT assay and Transwell invasion chambers were used to detect the inhibition rate and invasion ability of PC3 cells. And Western Blot was used to examined the expression of NF-kB, Snail, RKIP protein.Results:PC3 cells treated with KN93 for 24h showed a significantly decreased level of P-CaMK ? in each KN93 group when compared with control group(P<0.05). The inhibition rates of PC3 cells proliferation treated with KN93 for 24h were (6.88±1.79)%, (12.92±2.74)%, (17.88±2.86)%, (31.23±4.24)%. And the inhibition rates were(16.53±2.45)%, (29.02±1.74)%, (40.52±1.98)%, (52.26±3.51)%for PC3 cells treated with the inhibitor for 48h. The numbers of the PC3 cells traversing the membrane of the Transwell were (97±7)/HP, (59±9)/HP, (51±7)/HP, (24±3)/HP in KN93 groups and each was significantly decreased when compared with control group(149±17)/HP (P<0.01). Western Blot results showed that the expression of NF-?B P65 had no significant difference between control and KN93 groups(P>0.05), while the levels of P-NF-?B P65 and Snail were both obviously decreased after treated with KN93 for 24h(P<0.05). Instead, the protein expression of RKIP was remarkably increased by KN93 when compared with control groups(P<0.01).Conclusion:Inactivation of CaMK II can not only interfere with PC3 cell proliferation and invasion, but also affect the NF-?B/Snail/RKIP signaling pathway related to EMT. So, CaMK ? might be a upstream regulator fo this signaling pathway in PC3 cells. |
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