Zheng Y, Zhou J, Fu S Z, Fan J, Wu J B
Department of Oncology, The Affiliated Hospital of Luzhou Medical College, Luzhou, P.R.C.;
Third Military Medical University, Chongqin, P.R.C.
Curr Oncol. 2016 Feb;23(1):e35-40. doi: 10.3747/co.23.2844. Epub 2016 Feb 18.
Although the heart is one of the body's vital organs, with an abundant blood supply, metastasis to the heart is considered rare. In a previous study, we found that the myocardial microenvironment might contain a low molecular weight natural tumour suppressor. The present study was designed to investigate the inhibitory effect of cardiac myocyte-conditioned medium (cmcm) on the growth of A549 human lung adenocarcinoma cells in vitro and in vivo.
An mtt assay was used to detect the inhibition ratio with respect to A549 proliferation. Human lung adenocarcinoma cells (A549 cell strain) were transplanted subcutaneously into nude mice to produce tumours. The xenograft tumour growth in mice was observed after selected drug administration.
After treatment with cmcm and cisplatin (Cis), A549 cell viability significantly declined (p < 0.001). The cell viability in the cmcm and Cis groups were 53.42% ± 3.45% and 58.45% ± 6.39% respectively. Growth of implanted tumour cells in vivo was significantly inhibited in the cmcm group, the group treated with recombinant human adenovirus-p53, and the Cis-treated group compared with a control group. The inhibition rates were 41.44% in the cmcm group, 41.34% in the p53 group, and 64.50% in the Cis group. Lung metastasis capacity was significantly reduced in the presence of cmcm (p < 0.05). Lung metastasis inhibition rates in mice were 56.52% in the cmcm group, 47.83% in the p53 group, and 82.61% in the Cis group. With cmcm, the lives of A549-tumour-bearing mice could be significantly prolonged without any effect on weight loss.
Use of cmcm has the effect of reducing A549 cell viability, tumour volume, and lung metastasis rate, while prolonging survival duration without severe toxicity.
尽管心脏是人体重要器官之一,血液供应丰富,但心脏转移仍被认为较为罕见。在之前的一项研究中,我们发现心肌微环境可能含有一种低分子量天然肿瘤抑制因子。本研究旨在探讨心肌细胞条件培养基(cmcm)在体外和体内对A549人肺腺癌细胞生长的抑制作用。
采用MTT法检测cmcm对A549细胞增殖的抑制率。将人肺腺癌细胞(A549细胞株)皮下移植到裸鼠体内以形成肿瘤。在给予选定药物后观察小鼠体内异种移植肿瘤的生长情况。
用cmcm和顺铂(Cis)处理后,A549细胞活力显著下降(p<0.001)。cmcm组和Cis组的细胞活力分别为53.42%±3.45%和58.45%±6.39%。与对照组相比,cmcm组、重组人腺病毒-p53处理组和Cis处理组体内植入肿瘤细胞的生长均受到显著抑制。cmcm组的抑制率为41.44%,p53组为41.34%,Cis组为64.50%。在存在cmcm的情况下,肺转移能力显著降低(p<0.05)。cmcm组小鼠的肺转移抑制率为56.52%,p53组为47.83%,Cis组为82.61%。使用cmcm可显著延长荷A549肿瘤小鼠的生存期,且对体重减轻无任何影响。
使用cmcm具有降低A549细胞活力、肿瘤体积和肺转移率的作用,同时延长生存期且无严重毒性。