不同PTH、PTHrP多肽对MDA-MB-231乳腺癌细胞系增殖的影响  

Effects of different PTH and PTHrP polypeptides on the proliferation of MDA-MB-231 human breast carcinoma cell line

在线阅读下载全文

作  者:栾晓睿 严景 徐晨明 LUAN Xiaorui;YAN Jing;XU Chenming(Genetics Center of Obstetrics and Gynecology,Obstetrics&Gynecology Hospital of Fudan University,Shanghai 200011,China;Central Laboratory,Affiliated Xiaoshan Hospital,Hangzhou Normal University,Hangzhou,Zhejiang 311202,China)

机构地区:[1]复旦大学附属妇产科医院妇产科遗传中心,上海200011 [2]杭州师范大学附属萧山医院中心实验室,浙江杭州311202

出  处:《中国优生与遗传杂志》2022年第2期250-254,共5页Chinese Journal of Birth Health & Heredity

摘  要:目的探究甲状旁腺激素(PTH)1-34、甲状旁腺激素相关蛋白(PTHrP)1-33、PTHrP 1-36、PTHrP 1-86多肽对乳腺癌细胞系增殖的影响。方法使用多肽对乳腺癌细胞系MDA-MB-231进行处理。结果培养条件为2%FBS、处理时间为24 h时,PTH 1-34、PTHrP 1-33、PTHrP 1-36、PTHrP 1-86都对细胞增殖有显著抑制作用(P<0.001);加入PTHrP 1-86多肽处理48 h时,10 nmol/L、25 nmol/L处理组别对细胞增殖有促进作用(P<0.05)。结论本实验证明PTH 1-34、PTHrP 1-33、PTHrP 1-36、PTHrP 1-86皆对乳腺癌细胞系MDA-MB-231的生长有调控作用,可能参与细胞增殖的信号通路。长远来看,本研究有助于开发通过抑制乳腺癌细胞增殖进行癌症治疗的新疗法。Objective To analyze the effects of parathyroid hormone(PTH) 1-34, parathyroid hormone-related protein(PTHrP) 1-33, PTHrP 1-36, and PTHrP 1-86 peptides on the proliferation of human breast carcinoma cell line. Methods The human breast carcinoma cell line MDA-MB-231 were treated by peptides. Results PTH 1-34、PTHrP 1-33、PTHrP 1-36、PTHrP 1-86 inhibit cells proliferation significantly cultured in 2%FBS for 24 h(P<0.001). After treated for 48 h with 10 nmol/L, 25 nmol/L PTHrP 1-86, cells proliferation was significantly inhibited(P<0.05). Conclusion PTH 1-34, PTHrP 1-33,PTHrP 1-36, PTHrP 1-86 have regulatory effects on MDA-MB-231 cells proliferation. The peptides maybe involve in the signal pathway of cell proliferation. In the long run, this research could help develop new therapies for cancer by inhibiting the proliferation of breast cancer cells.

关 键 词:乳腺癌细胞系 多肽 细胞增殖 PTH PTHRP 

分 类 号:R737.9[医药卫生—肿瘤]

 

参考文献:

正在载入数据...

 

二级参考文献:

正在载入数据...

 

耦合文献:

正在载入数据...

 

引证文献:

正在载入数据...

 

二级引证文献:

正在载入数据...

 

同被引文献:

正在载入数据...

 

相关期刊文献:

正在载入数据...

相关的主题
相关的作者对象
相关的机构对象