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Effect and Mechanism of rhddADAM15 on the Proliferation of Bel-7402 Cells


Hou Ying, Chu Min, Wang Xiaomin, Chen Yun, Jin Jian*
Lab of Drug Design and Molecular Pharmacology, School of Pharmaceutical Sciences, Jiangnan University, Wuxi 214122, China
Abstract: ADAM15, a member of transmembrane proteins ADAMs, is over-expressed in many solid tumors such as breast, colorectal and ovarian cancer, playing important roles in the degradation of extracellular matrix, cell adhesion, intracellular signal transduction and pathological changes in tumors. Because of the RGD motif in its disintegrin domain, ADAM15 is considered to interact with integrins multifariously. We have established the recombinant human disintegrin domain of ADAM15 (rhddADAM15) by E.coli in our previous research. This study aimed at assessing the effect and mechanism of rhddADAM15 on the proliferation of Bel-7402 cells. rhddADAM15 inhibited the proliferation of Bel-7402 with an IC50 of 1.14 μmol/L by SRB assay. Bel-7402 cells had apoptotic amorphological nucleus changes using DAPI staining, and (87.44±7.25)% of Bel-7402 cells showed apoptotic features when treated with 6 μmol/L rhddADAM15 analyzed by PI staining. Moreover, partial S and G2/M arrests were observed on Bel-7402 cells. When treated with rhddADAM15 at the concentration of 4 μmol/L, the G0/G1 phase of Bel-7402 cells reduced by 14%. The level of CDC2 was down-regulated and the phosphorylation of CDC-Tyr15 was increased which aroused the G2/M arrest.


CSTR: 32200.14.cjcb.2014.04.0003