IGFBP7 contributes to epithelial-mesenchymal transition of HPAEpiC cells in response to radiation
Radiation-induced lung injury(RILI)frequently occurs in patients with thoracic malignancies.In re-sponse to radiation,alveolar epithelial cells(AEC)undergo epithelial-mesenchymal transition(EMT),contributing to the pathogenesisof RILI.The transforming growth factor-β1(TGF-β1)pathwayplays a crucial role radiation-induced EMT.Insulin like growth factor binding protein 7(IGFBP7)is reported as a downstream mediator of TGF-β1.In the present study,the levels of IGFBP7 and TGF-β1 were simultaneously increased in experimental RILI models and radiation-treated AEC(HPAEpic).The expression of IGFBP7 in radiation-treated HPAEpic cellswas obviously inhibited the spe-cific inhibitor of TGF-b receptor antagonist SB431542,and time-dependently enhanced byTGF-bl treatment.Moreover,IGFBP7 knockdown significantly attenuated the effects of radiation onmorphology change,the expression of EMT-related markers(E-cadherin,a-SMA andV imentin)and the phosphorylation of extracellular-signal-regulatedkinase(ERK).The effects of IGFBP7 overexpresion on the expression of EMT-related markerswere partially reversed by the ERK inhibitor-PD98059.In conclusion,IGFBP7,was enhanced byTGF-β1,may be involved in radiation-induced EMT of AEC via the ERK signaling pathway,thus contributing to the pathogenesis of RILI.
IGFBP7 EMT TGF-β1 ERK
ZHONG Ya-zhen LIN Ze-chen LU Jin-hua LIN Xian-lei WANG Nan LIN Sheng-you
Hangzhou Cancer Hospital The Second Clinical Medical College of Zhejiang University of Traditional Chinese Medicine GuangXing Hospital Affiliated to Zhejiang Chinese Medical University
国内会议
2018年浙江省中医药学会肿瘤分会、浙江省抗癌协会康复与姑息专委会学术年会
杭州
英文
97-103
2018-06-15（万方平台首次上网日期，不代表论文的发表时间）