CAJ | 학술논문

目的通过检测前列腺癌细胞中质子泵V-ATPase酶的相关基因和相关蛋白的表达，探讨V-ATPase酶抑制剂巴弗洛霉素A1在治疗前列腺癌转移中的潜在价值。方法检测前列腺癌细胞系PC3细胞中质子泵V-ATPase酶相关基因和相关蛋白表达水平；在此基础上，使用巴弗洛霉素A1刺激PC3细胞，观察前列腺癌细胞增殖、迁移和细胞内酸化等生物学行为变化。结果质子泵V-ATPase酶V-ATPaseV1A1、V-ATPase V1E和V-ATPase V0A1亚单位在PC3细胞内表达高于人骨髓间充质干细胞（BMSCs）细胞组，差异均有统计学意义（t分别=-13.78、-19.33、-13.45，P均＜0.05）。利用V-ATPase酶抑制剂巴弗洛霉素A1（10 nmol）处理96 h，仅有12.00±3.00％的前列腺癌细胞增殖，差异有统计学意义（t=37.17，P＜0.05）。与此同时，利用2.5 nmol巴弗洛霉素A1处理时，发生迁移的前列腺癌细胞数量从对照组的（233.33±20.55）个/孔，下降为（105.00±7.02）个/孔迁移，差异有统计学意义（t=8.07，P＜0.05）。进一步分子生物学机制分析表明，2.5 nmol巴弗洛霉素A1可完全抑制V-ATPase介导的酸化。结论应用巴弗洛霉素A1可使前列腺癌细胞酸化受影响，从而抑制前列腺癌细胞的增殖和迁移功能。
목적통과검측전렬선암세포중질자빙V-ATPase매적상관기인화상관단백적표체，탐토V-ATPase매억제제파불락매소A1재치료전렬선암전이중적잠재개치。방법검측전렬선암세포계PC3세포중질자빙V-ATPase매상관기인화상관단백표체수평；재차기출상，사용파불락매소A1자격PC3세포，관찰전렬선암세포증식、천이화세포내산화등생물학행위변화。결과질자빙V-ATPase매V-ATPaseV1A1、V-ATPase V1E화V-ATPase V0A1아단위재PC3세포내표체고우인골수간충질간세포（BMSCs）세포조，차이균유통계학의의（t분별=-13.78、-19.33、-13.45，P균＜0.05）。이용V-ATPase매억제제파불락매소A1（10 nmol）처리96 h，부유12.00±3.00％적전렬선암세포증식，차이유통계학의의（t=37.17，P＜0.05）。여차동시，이용2.5 nmol파불락매소A1처리시，발생천이적전렬선암세포수량종대조조적（233.33±20.55）개/공，하강위（105.00±7.02）개/공천이，차이유통계학의의（t=8.07，P＜0.05）。진일보분자생물학궤제분석표명，2.5 nmol파불락매소A1가완전억제V-ATPase개도적산화。결론응용파불락매소A1가사전렬선암세포산화수영향，종이억제전렬선암세포적증식화천이공능。
Objective To investigate the gene and protein expression of V-ATPase proton pump in prostate cancer cells and to explore the inhibitory effect of V-ATP proton pump inhibitor Bafilomycin A1 on prostate cancer metastasis. Meth-ods V-ATPase gene and protein expression were detected in prostate cancer cells (PC3). Bafilomycin A1 was used to stimulate PC3 cells. The proliferation assay, cell migration assay and acidification assay were observed. Results The V-ATPaseV1A1, V-ATPase V1E and V-ATPase V0A1 expression of V-ATP enzyme in PC3 cells was significantly higher than that of BMSCs (t=-13.78,-19.33,-13.45,P<0.05). Only about 12.00±3.00%of PC3 cells was proliferating after be-ing treated with bafilomycin A1 10 nmol for 96 hours which was significantly higher than before treatment (t=37.17,P<0.05). In addition, the migrated PC3 cells decreased from (233.33±20.55) per well in the control group to (105.00±7.02) per well in the group being treated with bafilomycin A1 at 2.5 nmol (t=8.07,P<0.05). Furthermore, bafilomycin A1 at 2.5nmol can completely inhibited intracellular acidification that mediated by V-ATPase. Conclusion Bafilomycin A1 can affect intracellular acidification of prostate cancer cells, thus restrain the proliferation assay, cell migration assay of prostate cancer cells.