RNA结合蛋白38基因对人乳腺癌BT474细胞生物学特性的影响

In vitro study of the effects of RNA binding motif protein 38 expression on the biological behavior of human breast cancer BT474 cells

目的观察RNA结合蛋白38（RNPCI）基因过表达对人乳腺癌细胞BT474的生物学特性的影响。方法细胞分为空白对照组、阴性对照组和实验组，采用慢病毒转染法，利用细胞计数试剂盒（CCK-8）法、平板克隆形成实验、Transwell小室实验观察其对BT474细胞生物学特性的影响。结果CCK-8实验显示，空白对照组、阴性对照组和实验组6d时吸光度（A）值分别为0．7147±0．0189、0．7708±0．0160、0．5568±0．0436（P〈0．05）。克隆形成实验显示，14d时细胞克隆形成数分别为（113．300±3．528）、（118．700±2．404）、（47．330±2．906）个（P〈0．01）。Transwell小室实验显示，实验组细胞24h迁移、侵袭实验中滤过膜细胞数分别为（61．670±4．842）、（14．670±1．856）个，均比空白对照组和阴性对照组降低（P〈0．01）。Westernblot法显示，过表达RNPCIa下调基质金属蛋白酶-2（MMP-2）的蛋白表达（P〈0．01）。结论RNPCIa基因可以抑制BT474细胞的生物学特性。RNPCIa与MMP-2的相互作用关系在乳腺癌的侵袭和转移中起调节作用。

Objective To investigate the effect of RNA binding motif protein 38 （ RNPC1 ） overexpression on the biological behavior of a human breast cancer cell line BT474. Methods Cell prolifera- tion was tested by cell counting kit 8 （CCK-8） assay. The ability of colony formation was tested by plate clone formation assay. The abilities of migration and invasion were evaluated by Transwell chambers. The relative expression of matrix metalloproteinase-2 （ MMP-2 ） protein was detected by Western blotting. Results CCK-8 test showed that the absorbance （A） value in experimental group, blank group and negative group at 6th day was （0. 714 7 ±0. 018 9） , （0. 770 8 ±0. 016 0） and （0. 556 8 ±0. 043 6） , respectively （P 〈 0. 05 ）. The colony formation number at 14th day was significantly less in experimental group （ 113. 300 ± 3. 528 ） than in blank group （ 118. 700 ± 2. 404 ） and negative group （47. 330 ± 2. 906 ） （ P 〈 0. 01 ）. The Transwell assay revealed that the number of cells passing through the Transwell membrance in experimental group [ （61. 670 ± 4. 842） for migration, and （ 14. 670 ± 1. 856） for invation± was significantly less than in blank group and control group （ both P 〈 0. 01 ）. Overexpression of RNPC1 a down-regulated the expression of MMP-2 protein. Conclusion RNPCla exhibits multiple antieancer functions in breast cancer cells. RNPCla interacts with MMP-2 to play an important role in the metastasis of breast cancer.