Fractionated radiotherapy might induce epithelial‐mesenchymal transition and radioresistance in a cellular context manner

Despite the fact that radiotherapy is a main therapeutic modality in cancer treatment, recent evidence suggests that fractionated radiotherapy (FR) might confer radioresistance through epithelial‐mesenchymal transition (EMT). Nevertheless, the effects of FR on EMT phenotype and the potential link be...

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Veröffentlicht in:Journal of cellular biochemistry 2019-05, Vol.120 (5), p.8601-8610
Hauptverfasser: Tahmasebi‐Birgani, Mohammad‐Javad, Teimoori, Ali, Ghadiri, Ata, Mansoury‐Asl, Halime, Danyaei, Amir, Khanbabaei, Hashem
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container_end_page 8610
container_issue 5
container_start_page 8601
container_title Journal of cellular biochemistry
container_volume 120
creator Tahmasebi‐Birgani, Mohammad‐Javad
Teimoori, Ali
Ghadiri, Ata
Mansoury‐Asl, Halime
Danyaei, Amir
Khanbabaei, Hashem
description Despite the fact that radiotherapy is a main therapeutic modality in cancer treatment, recent evidence suggests that fractionated radiotherapy (FR) might confer radioresistance through epithelial‐mesenchymal transition (EMT). Nevertheless, the effects of FR on EMT phenotype and the potential link between EMT induction and radioresistance development yet to be clarified. The aim of this study was to assess whether FR could promote EMT, and to elucidate if induction of EMT contributes to the acquisition of radioresistance. To this end, two human cancer cell lines (A549 and HT‐29) were irradiated (2 Gy/day) and analyzed using wound healing, transwell migration and invasion assays, real‐time polymerase chain reaction (for E‐cadherin, N‐cadherin, Vimentin, CD44, CD133, Snail, and Twist), clonogenic assay, Annexin V/PI, and 3‐[4,5‐dimethylthiazol‐2‐yl]‐2,5 diphenyl tetrazolium bromide (MTT) assay. Irradiation of A549 (for 5 or 10 consecutive days) resulted in morphological changes including elongation of cytoplasm and nuclei and pleomorphic nuclei. Also, irradiation‐enhanced migratory and invasive potential of A549. These phenotypic changes were in agreement with decreased expression of the epithelial marker (E‐cadherin), enhanced expression of mesenchymal markers (N‐cadherin, Vimentin, Snail, and Twist) and increased stemness factors (CD44 and CD133). Moreover, induction of EMT phenotype was accompanied with enhanced radioresistance and proliferation of irradiated A549. However, FR (for 5 consecutive days) did not increase HT‐29 motility. Furthermore, molecular alterations did not resemble EMT phenotype (downregulation of E‐cadherin, Vimentin, ALDH, CD44, CD133, and Snail). Eventually, FR led to enhanced radiosensitivity and decreased proliferation of HT‐29. Altogether, our findings suggest that FR might induce EMT and confer radioresistance in a cell context‐dependent manner. Ionizing radiation (IR) enhances the radioresistance of tumor cell lines in a cell context‐dependent manner. IR induces epithelial‐mesenchymal transition (EMT) in a cell context‐dependent manner. Radioresistance might be as a consequence of IR‐mediated EMT.
doi_str_mv 10.1002/jcb.28148
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Nevertheless, the effects of FR on EMT phenotype and the potential link between EMT induction and radioresistance development yet to be clarified. The aim of this study was to assess whether FR could promote EMT, and to elucidate if induction of EMT contributes to the acquisition of radioresistance. To this end, two human cancer cell lines (A549 and HT‐29) were irradiated (2 Gy/day) and analyzed using wound healing, transwell migration and invasion assays, real‐time polymerase chain reaction (for E‐cadherin, N‐cadherin, Vimentin, CD44, CD133, Snail, and Twist), clonogenic assay, Annexin V/PI, and 3‐[4,5‐dimethylthiazol‐2‐yl]‐2,5 diphenyl tetrazolium bromide (MTT) assay. Irradiation of A549 (for 5 or 10 consecutive days) resulted in morphological changes including elongation of cytoplasm and nuclei and pleomorphic nuclei. Also, irradiation‐enhanced migratory and invasive potential of A549. These phenotypic changes were in agreement with decreased expression of the epithelial marker (E‐cadherin), enhanced expression of mesenchymal markers (N‐cadherin, Vimentin, Snail, and Twist) and increased stemness factors (CD44 and CD133). Moreover, induction of EMT phenotype was accompanied with enhanced radioresistance and proliferation of irradiated A549. However, FR (for 5 consecutive days) did not increase HT‐29 motility. Furthermore, molecular alterations did not resemble EMT phenotype (downregulation of E‐cadherin, Vimentin, ALDH, CD44, CD133, and Snail). Eventually, FR led to enhanced radiosensitivity and decreased proliferation of HT‐29. Altogether, our findings suggest that FR might induce EMT and confer radioresistance in a cell context‐dependent manner. Ionizing radiation (IR) enhances the radioresistance of tumor cell lines in a cell context‐dependent manner. IR induces epithelial‐mesenchymal transition (EMT) in a cell context‐dependent manner. 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Nevertheless, the effects of FR on EMT phenotype and the potential link between EMT induction and radioresistance development yet to be clarified. The aim of this study was to assess whether FR could promote EMT, and to elucidate if induction of EMT contributes to the acquisition of radioresistance. To this end, two human cancer cell lines (A549 and HT‐29) were irradiated (2 Gy/day) and analyzed using wound healing, transwell migration and invasion assays, real‐time polymerase chain reaction (for E‐cadherin, N‐cadherin, Vimentin, CD44, CD133, Snail, and Twist), clonogenic assay, Annexin V/PI, and 3‐[4,5‐dimethylthiazol‐2‐yl]‐2,5 diphenyl tetrazolium bromide (MTT) assay. Irradiation of A549 (for 5 or 10 consecutive days) resulted in morphological changes including elongation of cytoplasm and nuclei and pleomorphic nuclei. Also, irradiation‐enhanced migratory and invasive potential of A549. 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subjects Annexin V
Apoptosis
Assaying
Cancer
cancer stem cell
CD44 antigen
Cytoplasm
E-cadherin
Elongation
epithelial‐mesenchymal transition
fractionated radiotherapy
Genotype & phenotype
Invasiveness
Irradiation
Mesenchyme
Nuclei
Phenotypes
Polyimide resins
Polymerase chain reaction
Radiation therapy
Radioresistance
Radiosensitivity
Tumor cell lines
Vimentin
Wound healing
title Fractionated radiotherapy might induce epithelial‐mesenchymal transition and radioresistance in a cellular context manner
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