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Chinese Journal of Oncology Prevention and Treatment ›› 2019, Vol. 11 ›› Issue (4): 303-307.doi: 10.3969/j.issn.1674-5671.2019.04.06

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Effect of bone marrow X-linked kinase on proliferation of cervical cancer cells and its potential #br# #br# mechanism#br#

  

  • Online:2019-08-25 Published:2019-09-17

Abstract: Objective To study the role of bone marrow X-linked kinase(BMX) on proliferation of human cervical cancer cells and its potential mechanism. Methods Clinical specimens of 34 cases of normal cervix,25 cases of cervical cancer in situ and 52 cases of invasive cervical cancer were collected from 2013 to 2017. Expression of BMX in different specimens was detected by immunohistochemistry. BMX-TALEN recombinant plasmid was transfected to construct a knockdown BMX-expressing cervical cancer cell line HeLa-BMX+/-. Cervical cancer cells HeLa-BMX+/- and HeLa-wild-type cells were cultured in complete medium containing inhibitor MK-2206 and rapamycin,respectively,and the cells cultured in DMSO medium were used as control group. The cell viability was detected by MTT analysis. The expression of BMX,Akt,p-Akt,mTOR and p-mTOR were detected by Western blot. Results The results of immunohistochemistry showed that the positive rate of BMX in normal cervix,cervical cancer in situ and invasive cervical cancer was statistically significant(26.5% vs 68.0% vs 88.5%,χ2=34.804,P<0.001),and there were statistical differences between the two groups(P<0.005). Low-expression BMX cervical cancer HeLa-BMX cells were successfully constructed. Western blot results showed that the expres-sion of BMX and p-Akt in HeLa-BMX+/- cells were lower than that in HeLa-wild-type cells(t=6.282,8.117,P<0.001),while the expression of total Akt was similar(t=2.035,P=0.126). Compared with the control group,the expression of p-Akt and p-mTOR in HeLa-wild-type and HeLa-BMX+/- cells treated with MK-2206 and rapamycin were inhibited. Conclusion BMX can promote the proliferation of cervical cancer cells,which may be related to the inhibition of PI3K/AKT/mTOR signaling pathway.

Key words: Cervical cancer, Bone marrow X-linked kinase, Proliferation, PI3K/AKT/mTOR signaling pathway, Mechanism

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