scholarly journals Regulation of Ionizing Radiation-Induced Adhesion of Breast Cancer Cells to Fibronectin by Alpha5beta1 Integrin

2014 ◽  
Vol 181 (6) ◽  
pp. 650-658 ◽  
Author(s):  
Shin Hee Lee ◽  
Huiwen Cheng ◽  
Ye Yuan ◽  
Shiyong Wu
2019 ◽  
Vol 39 (4) ◽  
Author(s):  
Xuguang Hu ◽  
Dan Ding ◽  
Jiayi Zhang ◽  
Jianguo Cui

Abstract Radiotherapy is a major therapeutic strategy for breast cancer, while cancer radioresistance remains an obstacle for the successful control of the tumor. Novel radiosensitizing targets are to be developed to overcome radioresistance. Recently, long non-coding RNAs (lncRNAs) were proved to play critical roles in cancer progression. Among all, lncRNA HOTAIR was found to participate in cancer metastasis and chemoresistance. In the present study, we aimed to investigate the radiosensitizing effects of targeting HOTAIR and the underlying mechanism. Our data showed that HOTAIR (HOX antisense intergenic RNA) was up-regulated in breast cancer cells and tissues, and the expression of HOTAIR increased following irradiation. Knockdown of HOTAIR inhibited cell survival and increased cell apoptosis in response to ionizing radiation. Moreover, compared with control group, radiation induced more DNA damage and cell cycle arrest in HOTAIR knockdown cells. Finally, we found that the radiosentizing effects of HOTAIR were related to the up-regulation of miR-218, a ceRNA of HOTAIR. In conclusion, our finding showed that HOTAIR inhibition sensitizes breast cancer cells to ionizing radiation, induced severe DNA damage and activated apoptosis pathways, suggesting a possible role of HOTAIR as a novel target for breast cancer radiosensitization.


2018 ◽  
Vol 107 ◽  
pp. 606-614 ◽  
Author(s):  
Yan Wang ◽  
Yuxuan Wang ◽  
Sihong Liu ◽  
Yamin Liu ◽  
Huihua Xu ◽  
...  

2015 ◽  
Vol 46 (4) ◽  
pp. 1659-1666 ◽  
Author(s):  
MIN YOUNG KIM ◽  
SEONG-JOON PARK ◽  
JAE WOONG SHIM ◽  
KWANGMO YANG ◽  
HO SUNG KANG ◽  
...  

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Jiraporn Kantapan ◽  
Siwaphon Paksee ◽  
Aphidet Duangya ◽  
Padchanee Sangthong ◽  
Sittiruk Roytrakul ◽  
...  

Abstract Background Radioresistance can pose a significant obstacle to the effective treatment of breast cancers. Epithelial–mesenchymal transition (EMT) is a critical step in the acquisition of stem cell traits and radioresistance. Here, we investigated whether Maprang seed extract (MPSE), a gallotannin-rich extract of seed from Bouea macrophylla Griffith, could inhibit the radiation-induced EMT process and enhance the radiosensitivity of breast cancer cells. Methods Breast cancer cells were pre-treated with MPSE before irradiation (IR), the radiosensitizing activity of MPSE was assessed using the colony formation assay. Radiation-induced EMT and stemness phenotype were identified using breast cancer stem cells (CSCs) marker (CD24−/low/CD44+) and mammosphere formation assay. Cell motility was determined via the wound healing assay and transwell migration. Radiation-induced cell death was assessed via the apoptosis assay and SA-β-galactosidase staining for cellular senescence. CSCs- and EMT-related genes were confirmed by real-time PCR (qPCR) and Western blotting. Results Pre-treated with MPSE before irradiation could reduce the clonogenic activity and enhance radiosensitivity of breast cancer cell lines with sensitization enhancement ratios (SERs) of 2.33 and 1.35 for MCF7 and MDA-MB231cells, respectively. Pretreatment of breast cancer cells followed by IR resulted in an increased level of DNA damage maker (γ-H2A histone family member) and enhanced radiation-induced cell death. Irradiation induced EMT process, which displayed a significant EMT phenotype with a down-regulated epithelial marker E-cadherin and up-regulated mesenchymal marker vimentin in comparison with untreated breast cancer cells. Notably, we observed that pretreatment with MPSE attenuated the radiation-induced EMT process and decrease some stemness-like properties characterized by mammosphere formation and the CSC marker. Furthermore, pretreatment with MPSE attenuated the radiation-induced activation of the pro-survival pathway by decrease the expression of phosphorylation of ERK and AKT and sensitized breast cancer cells to radiation. Conclusion MPSE enhanced the radiosensitivity of breast cancer cells by enhancing IR-induced DNA damage and cell death, and attenuating the IR-induced EMT process and stemness phenotype via targeting survival pathways PI3K/AKT and MAPK in irradiated breast cancer cells. Our findings describe a novel strategy for increasing the efficacy of radiotherapy for breast cancer patients using a safer and low-cost natural product, MPSE.


2017 ◽  
Vol 193 (10) ◽  
pp. 848-855 ◽  
Author(s):  
Takamitsu Hara ◽  
Manabu Iwadate ◽  
Kazunoshin Tachibana ◽  
Satoshi Waguri ◽  
Seiichi Takenoshita ◽  
...  

2012 ◽  
Vol 30 (4) ◽  
pp. 1008-1016 ◽  
Author(s):  
Zhongxing Liang ◽  
Jeffrey Ahn ◽  
Donna Guo ◽  
John R. Votaw ◽  
Hyunsuk Shim

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