scholarly journals Paired‑related homeobox 1 overexpression promotes multidrug resistance via PTEN/PI3K/AKT signaling in MCF‑7 breast cancer cells

2020 ◽  
Author(s):  
Haoyue Luo ◽  
Shaobo Cong ◽  
Jiaojiao Dong ◽  
Litao Jin ◽  
Dandan Jiang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Multidrug Resistance ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Akt Signaling ◽  
Mcf 7

scholarly journals Induction of multidrug resistance associated protein 2 in tamoxifen-resistant breast cancer cells

2007 ◽  
Vol 14 (2) ◽  
pp. 293-303 ◽  
Author(s):  
Hoo Kyun Choi ◽  
Jin Won Yang ◽  
Sang Hee Roh ◽  
Chang Yeob Han ◽  
Keon Wook Kang
Keyword(s):  
Breast Cancer ◽  
Multidrug Resistance ◽  
Cancer Cells ◽  
Transcriptional Activation ◽  
Breast Cancer Cells ◽  
Pregnane X Receptor ◽  
Pi3 Kinase ◽  
Gene Promoters ◽  
Breast Cancer Patients ◽  
Mcf 7

Acquired resistance to tamoxifen (TAM) is a serious therapeutic problem in breast cancer patients. The transition from chemotherapy-responsive breast cancer cells to chemotherapy-resistant cancer cells is mainly accompanied by the increased expression of multidrug resistance-associated proteins (MRPs). In this study, it was found that TAM-resistant MCF-7 (TAMR-MCF-7) cells expressed higher levels of MRP2 than control MCF-7 cells. Molecular analyses using MRP2 gene promoters supported the involvement of the pregnane X receptor (PXR) in MRP2 overexpression in TAMR-MCF-7 cells. Although CCAAT/enhancer-binding protein β was overexpressed continuously in TAMR-MCF-7 cells, this might not be responsible for the transcriptional activation of the MRP2 gene. In addition, the basal activities of phosphatidylinositol 3-kinase (PI3-kinase) were higher in the TAMR-MCF-7 cells than in the control cells. The inhibition of PI3-kinase significantly reduced both the PXR activity and MRP2 expression in TAMR-MCF-7 cells. Overall, MRP2 induction plays a role in the additional acquisition of chemotherapy resistance in TAM-resistant breast cancer.

Genistein induces apoptosis by the inactivation of the IGF-1R/p-Akt signaling pathway in MCF-7 human breast cancer cells

2015 ◽  
Vol 6 (3) ◽  
pp. 995-1000 ◽  
Author(s):  
Jun Chen ◽  
Yuxin Duan ◽  
Xing Zhang ◽  
Yu Ye ◽  
Bo Ge ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Akt Signaling ◽  
Human Breast Cancer Cells ◽  
Akt Signaling Pathway ◽  
Human Breast ◽  
Anti Cancer ◽  
Mcf 7

Genistein is an estrogenic soy-derived compound belonging to the isoflavone class and shows anti-cancer effects.

scholarly journals Ginsenoside induces cell death in breast cancer cells via ROS/PI3K/Akt signaling pathway

2020 ◽  
Vol 19 (8) ◽  
pp. 1631-1636
Author(s):  
Lihong He ◽  
Xiaorui Wang ◽  
Qing Ma ◽  
Weipeng Zhao ◽  
Yongsheng Jia ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Mechanism Of Action ◽  
Breast Cancer Cells ◽  
Akt Signaling ◽  
Control Group ◽  
Akt Signaling Pathway ◽  
Protein Expressions ◽  
Mcf 7

Purpose: To study the influence of ginsenoside on breast carcinoma, and the mechanism of action involved.Methods: Different concentrations of ginsenoside were used to treat MCF-7 breast cancer cell line. Cell viability was measured by MTT assay, while protein expressions of p-Akt and p-PI3K were determined using Western blotting. The concentrations of reactive oxidative reactants and reactive oxygen species (ROS) were assessed using fluorescence immunoassay and immunofluorescence assay. The mechanism of action involved in ginsenoside-mediated apoptosis was determined based on ROS/PI3K/Akt signaling pathway.Results: There was no change in the inhibition of MCF-7 cell proliferation in control cells with time (p > 0.05). However, inhibition of MCF-7 cell proliferation in ginsenoside group was significantly higher than that in the control group (p < 0.05); furthermore, it increased with time and ginsenoside concentration. Apoptosis was markedly and concentration-dependently higher in ginsenoside-treated MCF-7 cells than in controls (p > 0.05). There were lower protein levels of p-PI3K and p-Akt in ginsenoside-exposed MCF-7 cells than in control group; the protein expressions  decreased with increase in ginsenoside concentration (p < 0.05). The expressions of ROS in ginsenoside-treated MCF-7 cells declined, relative to the untreated group; in addition, the expressions decreased with increase in ginsenoside concentration (p < 0.05).Conclusion: Ginsenoside suppresses proliferation of MCF-7 cell line, and exerts apoptotic effect on the cells via inhibition of the ROS/PI3K/Akt signal pathway. This provides a new approach to treat breast cancer. Keywords: Breast cancer cells, Ginsenoside, Apoptosis, ROS/PI3K/Akt signaling pathway

scholarly journals Knockdown of lncRNA FOXD2-AS1 Inhibits Proliferation, Migration, and Drug Resistance of Breast Cancer Cells

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Qiaohong Nong ◽  
Shaokang Yu ◽  
Hui Hu ◽  
Xue Hu
Keyword(s):  
Breast Cancer ◽  
Drug Resistance ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Breast Cancer Cells ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Invasion And Migration ◽  
And Migration ◽  
Mcf 7

Objective. In order to investigate the effect of lncRNA FOXD2-AS1 on breast cancer cells proliferation, migration, and drug resistance as well as its molecular mechanism. Methods. Real-time PCR was used to detect the expression of breast cancer tissues and cells from patients admitted to our hospital and the expression of lncRNA FOXD2-AS1 in MCF-7/ADR in adriamycin- (ADR-) resistant breast cancer cells. After interfering with or overexpressing lncRNA FOXD2-AS1 in MCF-7/ADR cells, cell proliferation, apoptosis, invasion, and migration were detected using CCK-8, flow cytometry, Transwell assay, and scratch test, respectively. The protein levels of PI3K, p-PI3K, AKT, and p-AKT in the PI3K/AKT signaling pathway were detected by Western blot. Results. lncRNA FOXD2-AS1 was upregulated in breast cancer tissues and cells and increased cell drug resistance to ADR. Downregulation of lncRNA FOXD2-AS1 inhibited invasion and migration of MCF-7/ADR cells, promoted apoptosis, increased chemosensitivity of MCF-7/ADR cells, and inhibited the activity of PI3K/AKT signaling pathway in MCF-7/ADR cells. Conclusions. lncRNA FOXD2-AS1 can promote the proliferation, invasion, migration, and drug resistance of breast cancer cells, inhibit apoptosis, and accelerate the development of breast cancer by positively regulating the PI3K/AKT signaling pathway.

Sign in / Sign up

Export Citation Format

Share Document