scholarly journals Mechanical stress-induced cell death in breast cancer cells

Biology Open ◽  
2019 ◽  
Vol 8 (8) ◽  
pp. bio043133 ◽  
Author(s):  
Satomi Takao ◽  
Minoru Taya ◽  
Cerwyn Chiew
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Mechanical Stress ◽  
Breast Cancer Cells

Oxyresveratrol drives caspase-independent apoptosis-like cell death in MDA-MB-231 breast cancer cells through the induction of ROS

2020 ◽  
Vol 173 ◽  
pp. 113724 ◽  
Author(s):  
Damu Sunilkumar ◽  
G. Drishya ◽  
Aneesh Chandrasekharan ◽  
Sanu K. Shaji ◽  
Chinchu Bose ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Breast Cancer Cells

scholarly journals Laser nanobubbles induce immunogenic cell death in breast cancer

Nanoscale ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 3644-3653
Author(s):  
Hieu T. M. Nguyen ◽  
Nitesh Katta ◽  
Jessica A. Widman ◽  
Eri Takematsu ◽  
Xu Feng ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Dendritic Cell ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Cell Activation ◽  
Immunogenic Cell Death ◽  
Dendritic Cell Activation

Laser nanobubbles induce dendritic cell activation in breast cancer cells.

Identification of Two Novel Thiophene Analogues as Inducers of Autophagy Mediated Cell Death in Breast Cancer Cells

2021 ◽  
pp. 116112
Author(s):  
Chandrima Gain ◽  
Aparna Sarkar ◽  
Shrea Bural ◽  
Moumita Rakshit ◽  
Jeet Banerjee ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Breast Cancer Cells

scholarly journals A radiosensitizer, gallotannin-rich extract from Bouea macrophylla seeds, inhibits radiation-induced epithelial-mesenchymal transition in breast cancer cells

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Jiraporn Kantapan ◽  
Siwaphon Paksee ◽  
Aphidet Duangya ◽  
Padchanee Sangthong ◽  
Sittiruk Roytrakul ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Dna Damage ◽  
Cell Death ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Breast Cancer Cell Lines ◽  
Mesenchymal Transition ◽  
Mammosphere Formation ◽  
Radiation Induced

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.

Inhibition of sirtuin 1 deacetylase by miR-211-5p provides a mechanism for the induction of cell death in breast cancer cells

Gene ◽  
2019 ◽  
Vol 711 ◽  
pp. 143939 ◽  
Author(s):  
Sahar Yarahmadi ◽  
Zohreh Abdolvahabi ◽  
Zahra Hesari ◽  
Masoumeh Tavakoli-Yaraki ◽  
Zeynab Yousefi ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Sirtuin 1

IFT20 confers paclitaxel resistance by triggering β-arrestin-1 to modulate ASK1 signaling in breast cancer

2021 ◽  
Author(s):  
Ni Qiu ◽  
Huan Jin ◽  
Lulu Cui ◽  
Yong-tao Zhan ◽  
Hao-ming Xia ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Molecular Mechanism ◽  
Breast Cancer Cells ◽  
Feedback Inhibition ◽  
In Vivo Studies ◽  
Paclitaxel Resistance ◽  
Western Blots ◽  
Paclitaxel Treatment

Abstract Background: System paclitaxel-based chemotherapy is the first-line treatment regimen of defense against breast cancer, but inherent or acquired chemotherapy resistance remains a major obstacle in breast cancer therapy. Elucidating the molecular mechanism of chemoresistance is essential to improve the outcome of patients with breast cancer. Methods: Paclitaxel sensitivity was first evaluated using models of IFT20 deletion and overexpression of breast cancer cells in vitro and in vivo studies to identify the effect of IFT20 on paclitaxel chemoresistance. To delineate the molecular mechanism of IFT20 contributions to paclitaxel chemoresistance, changes in ASK signaling and its downstream JNK cascades expression were quantified using western blots, and the potential involvement of β-arrestin-1 was investigated using co-IP studies. Results: IFT20 is positively associated with shorter relapse-free survival in patients with system paclitaxel-based chemotherapy. High expressed IFT20 in breast cancer cells increases resistance to cell death upon paclitaxel treatment; in contrast, IFT20 knockdown enhances apoptosis in breast cancer cells in response to paclitaxel. Mechanistically, IFT20 triggers β-arrestin-1 to bind with ASK1 and promotes the ubiquitination of ASK1 degradation, leading to attenuating ASK1 signaling and its downstream JNK cascades, which helped cells to escape from cell death during paclitaxel treatment. Conclusion: IFT20 confers to paclitaxel chemoresistance. It interacts with β-arrestin-1 to mediate ubiquitination of ASK1 for feedback inhibition of ASK1/JNK signaling and restrains paclitaxel-induced apoptosis. These findings identify IFT20 as a promising novel target for overcoming paclitaxel resistance in breast cancer.

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