title: MicroRNA-144 affects radiotherapy sensitivity by promoting proliferation, migration and invasion of breast cancer cells.
abstract: Radiotherapy resistance remains a major obstacle for patients with breast cancer. miRNAs are important regulators in many biological processes including proliferation, apoptosis, invasion and metastasis and response to treatment in different types of tumors. Here, we describe the role of miRNA-144 in the regulation of radiotherapy sensitivity, migration and invasion of breast cancer cells. The cell survival rate of breast cancer cells was measured by WST-1 assay after irradiation. The caspase-3/-7 activity and apoptotic proteins were analyzed by Caspase-Glo3/7 assay and western blot analysis, respectively. The migration and invasion of breast cancer cells were evaluated by BD Transwell migration and Matrigel invasion assays. The EMT markers were detected by western blot analysis. We found that overexpression of miR-144 increased the proliferation rate of MDA-MB-231 cells without radiation. Both MDA-MB‑231 and SKBR3 cells exhibited significantly increased radiation resistance after overexpression of miR-144. Meanwhile, the migration and invasion of both MDA-MB-231 and SKBR3 cells were changed by altered miR-144 expression. In addition, the overexpression of miR-144 inhibited E-cadherin expression and promoted Snail expression. miR-144 activated AKT by downregulation of PTEN in breast cancer cells. Our results strongly suggest that miR-144 acts as an important regulator of tumorigenesis and tumor progression of breast cancer. These results indicate that miR-144 might serve as a potential molecular target for breast cancer treatment.
authors.affiliation: Department of Tumor Radiation Therapy, The Second Hospital of Jilin University, Changchun, Jilin, P.R. China.
authors.forename: Lei
authors.initials: L
authors.lastname: Yu
authors.affiliation: Department of Tumor Radiation Therapy, The Second Hospital of Jilin University, Changchun, Jilin, P.R. China.
authors.forename: Yanming
authors.initials: Y
authors.lastname: Yang
authors.affiliation: Department of Tumor Radiation Therapy, The Second Hospital of Jilin University, Changchun, Jilin, P.R. China.
authors.forename: Jiguang
authors.initials: J
authors.lastname: Hou
authors.affiliation: Department of Tumor Radiation Therapy, The Second Hospital of Jilin University, Changchun, Jilin, P.R. China.
authors.forename: Chengwei
authors.initials: C
authors.lastname: Zhai
authors.affiliation: Department of Tumor Radiation Therapy, The Second Hospital of Jilin University, Changchun, Jilin, P.R. China.
authors.forename: Yunhao
authors.initials: Y
authors.lastname: Song
authors.affiliation: Department of Tumor Radiation Therapy, The Second Hospital of Jilin University, Changchun, Jilin, P.R. China.
authors.forename: Zhiliang
authors.initials: Z
authors.lastname: Zhang
authors.affiliation: Department of Tumor Radiation Therapy, The Second Hospital of Jilin University, Changchun, Jilin, P.R. China.
authors.forename: Ling
authors.initials: L
authors.lastname: Qiu
authors.affiliation: Department of Tumor Radiation Therapy, The Second Hospital of Jilin University, Changchun, Jilin, P.R. China.
authors.forename: Xiaojing
authors.initials: X
authors.lastname: Jia
mesh_terms: D017209:Apoptosis / Q000235:genetics; D001943:Breast Neoplasms / Q000235:genetics* / Q000473:pathology / Q000532:radiotherapy; D015820:Cadherins / Q000096:biosynthesis; D053148:Caspase 3 / Q000096:biosynthesis; D045744:Cell Line, Tumor; D002465:Cell Movement / Q000235:genetics; D049109:Cell Proliferation / Q000235:genetics*; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D035683:MicroRNAs / Q000096:biosynthesis* / Q000235:genetics; D009361:Neoplasm Invasiveness / Q000235:genetics / Q000473:pathology; D051059:PTEN Phosphohydrolase / Q000096:biosynthesis; D011836:Radiation Tolerance / Q000235:genetics*
chemical_list: D015820:Cadherins; C554293:MIRN144 microRNA, human; D035683:MicroRNAs; D051059:PTEN Phosphohydrolase; C494929:PTEN protein, human; D053148:Caspase 3