详细信息

LIF Inhibits Proliferation of Esophageal Squamous Carcinoma Cells by Radiation Mediated Through JAK-STAT Signaling Pathway  ( SCI-EXPANDED收录)  

文献类型:期刊文献

英文题名:LIF Inhibits Proliferation of Esophageal Squamous Carcinoma Cells by Radiation Mediated Through JAK-STAT Signaling Pathway

作者:Luo, Hongtao[1,3];Yang, Zhen[1,2];Zhang, Qiuning[1,3];Li, Tingdong[4];Liu, Ruifeng[1,3];Feng, Shuangwu[1];Liu, Zhiqiang[1,3];Sun, Shilong[1,3];Chen, Junru[1];Wang, Xiaohu[1,3,4];Xie, Xiaoling[5]

第一作者:Luo, Hongtao

通信作者:Wang, XH[1];Wang, XH[2];Wang, XH[3]

机构:[1]Chinese Acad Sci, Inst Modern Phys, Lanzhou, Peoples R China;[2]Gansu Univ Chinese Med, Sch Publ Hlth, Lanzhou, Peoples R China;[3]Lanzhou Heavy Ion Hosp, Lanzhou, Peoples R China;[4]Gansu Prov Canc Hosp, Lanzhou, Peoples R China;[5]Lanzhou Univ, Hosp 1, Cent Lab, Lanzhou, Peoples R China

第一机构:Chinese Acad Sci, Inst Modern Phys, Lanzhou, Peoples R China

通信机构:[1]corresponding author), Chinese Acad Sci, Inst Modern Phys, Lanzhou, Peoples R China;[2]corresponding author), Lanzhou Heavy Ion Hosp, Lanzhou, Peoples R China;[3]corresponding author), Gansu Prov Canc Hosp, Lanzhou, Peoples R China.

年份:2023

卷号:14

期号:4

起止页码:532

外文期刊名:JOURNAL OF CANCER

收录:;Scopus(收录号:2-s2.0-85152204265);WOS:【SCI-EXPANDED(收录号:WOS:000942510400001)】;

基金:Funding The study was supported by the National Key Research and Development Program of China (No. 2022YFC2401500) , Science and Technology Plan Project of Chengguan District of Lanzhou (No. 2020-2-2-5) , Talent Innovation and Venture Project of Lanzhou City (No. 2021-RC-125; 2020-RC-113) , China Foundation for International Medical Exchange (No. Z-2017-24-2108) , and Gansu Province Project of Science and Technologies (Grant No. 20JR10RA680) .

语种:英文

外文关键词:Carbon ion; Esophageal squamous cell carcinoma; Proteomics; LIF

摘要:Background: Esophagus cancer is a malignant tumor with a high incidence rate, and radiation is an important modality for esophageal cancer therapy. However, therapeutic failure in the treatment of ESCC is often attributed to an inherent radio-resistance of the tumor cells. This study discusses effect and mechanism of carbon ion exerts tumor-inhibiting proliferation via down-regulation of LIF in esophageal squamous cell carcinoma.Methods: Colony formation, CCK8 and EdU assays were used to detect cell survival and proliferation after 0 and 2Gy carbon ion irradiation of ECA109 cells. Proteomics changes were probed in response to carbon ion irradiation using quantitative proteomics approach incorporating TMT isotope tags. Then, candidate genes were identified via bioinformatics analysis methods and microarray results were verified by real-time qPCR. Paired ESCC tumor tissues and adjacent non-tumor samples from 17 patients were collected and used for detecting expression by immunohistochemistry. Furthermore, small interfering RNA (siRNA) was transfected into ECA109 and KYSE150 cells and cell proliferation was analyzed by EdU assay. Flow cytometry and Western blot were performed to measure the and apoptosis and JAK-STAT3 protein expression level of ECA109 and KYSE150 cells combined drugs after siLIF transfection.Results: When compared with the control (0Gy), Inhibition of ECA109 cell proliferation and clonogenic survival by 2 Gy carbon ions, radiation group screened 360 differentially expressed proteins, 156 of which were up-regulated and 144 were down-regulated. Downregulation of LIF expression by siRNA enhances apoptotic in the ECA109 and KYSE150 cells, significantly inhibited esophageal squamous cell carcinoma cells proliferation. In ESCC cells, the JAK/STAT3 signaling pathway is inhibited in a LIF-dependent manner, resulting in the expression of STAT3 downstream target genes. Carbon ions combined with siLIF inhibited cell proliferation more significantly. The inhibitory cell proliferation effect was more pronounced by the combined intervention of carbon ion irradiation with siLIF. LIF expression was 18.51 +/- 9.84 and 5.82 +/- 4.50 in 17 paired ESCC tissues and adjacent non-cancerous tissues, respectively. LIF protein expression was lower in ESCC than in the adjacent normal tissue.Conclusion: The findings of this study reveal that Carbon ion knockdown was shown to downregulate LIF in ESCC cells. LIF is involved in ESCC proliferation and inhibited the ESCC cell proliferation by activating the STAT3 signaling pathways.

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