Realationship study on miRNA-675-5p and epithelial-mesenchymal transition in esop-hageal squamous cell carcinoma
ZHANG Qian1 SUN Yonghong1 WEN Shimin1 QUAN Yaping1 BIE Jun1 FU Xi2
1.Department of Oncology, Nanchong Central Hospital the Second Affiliated Medical College of North Sichuan Medical Collage, Sichuan Province, Nanchong 637000, China;
2.Department of Oncology, Pidu District People′s Hospital of Chengdu City, Sichuan Province, Chengdu 611730, China
Abstract：Objective To investigated the correlation between the expression of miRNA-675-5p and epithelial-mesenchymal transition (EMT) in esophageal squamous cell carcinoma (ESCC). Methods Real-time quantitative PCR was used to detect the differential expression of miRNA-675-5p in ESCC and normal adjacent tissues, while the correlation between its expression level and clinical stage of patients was analyzed. Liposomes was transfected into ECA109 cell, and divided into miR-675-recursor group, miR-675-5p-inhibition group and NC group. The expression of miRNA-675-5p was up-regulated and inhibited, while the effect of changing the expression of the target gene on the migration and invasion of ECA109 cell lines was analyzed. The expression levels of E-cadherin, N-cadherin, and Vimentin in EMT-associated proteins in each group of cells were detected by western blot experiments, while the effect on the EMT process of ECA109 strain was evaluated. Results Compared with normal adjacent tissues, miRNA-675-5p expression was significantly increased in ESCC tissues (P ＜ 0.05), and comparison of miRNA-675-5p expression in patients with different stages, the differences were statistically significant (P ＜ 0.05). Compared with the NC group, the miR-675-recursor group had significantly enhanced cell migration and invasion ability, and the miR-675-5p-inhibition group had significantly reduced cell migration and invasion ability (P ＜ 0.05). In addition, compared with the NC group, the expression of E-cadherin protein in the miR-675-recursor group was reduced, while the expression of N-cadherin and Vimentin proteins were increased; the expression of E-cadherin protein in the miR-675-5p-inhibition group was increased, while the expression of N-cadherin and Vimentin proteins were reduced (P ＜ 0.05). Conclusion The expression of miRNA-675-5p is related to the TNM stage of ESCC patients. miR-675-5p can promote the interstitial transformation of ESCC cells and thus enhance the invasion ability; down-regulated expression can reverse the EMT process of ESCC cells and reduce the migration and invasion ability.
[1] 曹小琴，孙喜斌.食管癌发病水平及变化趋势[J].中国肿瘤临床，2016，4（21）：932-936.
[2] Hesari A，Azizian M，Sheikhi A，et al. Chemopreventive and therapeutic potential of curcumin in esophageal cancer：Current and future status [J]. IJC，2019，144（6）：1215-1226.
[3] 中华人民共和国国家健康委员会.食管癌诊疗规范（2018年版）[DB/OL].2018：1-69.
[4] Costa V，Lo Dico A，Rizzo A，et al. MiR-675-5p supports hypoxia induced epithelial to mesenchymal transition in colon cancer cells [J]. Oncotarget，2017，8（15）：24292-24302.
[5] Cui J，Mo J，Luo M，et al. c-Myc-activated long non-coding RNA H19 downregulates miR-107 and promotes cell cycle progression of non-small cell lung cancer [J]. Int J Clin Exp Pathol，2015，8（30）：12400-12409.
[6] Li S，Yu Z，Chen SS，et al. The YAP1 oncogene contributes to bladder cancer cell proliferation and migration by regulating the H19 long noncoding RNA [J]. Urol Oncol，2015， 33（427）：165-174.
[7] Zhou WA-Ohoo，Ye XL，Xu J，et al. The lncRNA H19 mediates breast cancer cell plasticity during EMT and MET plasticity by differentially sponging miR-200b/c and let-7b [J]. Sci Signal，2017，10（483）：678-682.
[8] Zhuang M，Gao W，Xu J，et al. The long non-coding RNA H19-derived miR-675 modulates human gastric cancer cell proliferation by targeting tumor suppressor RUNX1 [J]. Biochem Biophys Res Commun，2014，448（4）：121-129.
[9] Liu FT，Pan H，Xia GF，et al. Prognostic and clinicopathological significance of long noncoding RNA H19 overexpression in human solid tumors：evidence from a meta-analysis [J]. Oncotarget，2016，7（50）：83177-83186.
[10] Tsang WP，Ng EK，Ng SS，et al. Oncofetal H19-derived miR-675 regulates tumor suppressor RB in human colorectal cancer [J]. Carcinogenesis，2010，31（3）：350-358.
[11] 张航.Hsa-miR-675-5p在食管鳞癌中的表达及其功能机制研究[D].长沙：中南大学，2013.
[12] Lagergren J，Smyth E，Cunningham D，et al. Oesophageal cancer [J]. The Lancet，2017，390（100）：2383-2396.
[13] Matouk IJ，Halle D，Raveh E，et al. The role of the oncofetal H19 lncRNA in tumor metastasis：orchestrating the EMT-MET decision [J]. Oncotarget，2016，7（11）：3748-3765.
[14] Zhang X，Hamblin MH，Yin KJ. The long noncoding RNA Malat1：Its physiological and pathophysiological functions [J]. RNA Biol，2017，14（12）：1705-1714.
[15] Hosseinahli N，Aghapour M. Treating cancer with microRNA replacement therapy：A literature review [J]. J Cell Physio，2018，233（8）：5574-5588.
[16] Tripathi V，Ellis JD，Shen Z，et al. The nuclear-retained noncoding RNA MALAT1 regulates alternative splicing by modulating SR splicing factor phosphorylation [J]. Mol Cell，2010，39（6）：925-938.
[17] Vahidian F，Mohammadi H. MicroRNAs and breast cancer stem cells：Potential role in breast cancer therapy [J]. J Cell Physio，2019，234（4）：3294-3306.
[18] Chaffer CL，San Juan BP，Lim E，et al. EMT，cell plasticity and metastasis [J]. Cancer Metastasis Rev，2016，35（4）：645-654.
[19] Brabletz T，Kalluri R，Nieto MA，et al. EMT in cancer [J]. Nat Rev Cancer，2018，18（2）：128-134.
[20] O′Brien SJ，Carter JV，Burton JF，et al. The role of the miR-200 family in epithelial-mesenchymal transition in colorectal cancer：a systematic review [J]. Int J Cancer，2018，142（12）：2501-2511.
2020, Vol. 17 
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