scholarly journals The LQB-223 Compound Modulates Antiapoptotic Proteins and Impairs Breast Cancer Cell Growth and Migration

2019 ◽  
Vol 20 (20) ◽  
pp. 5063
Author(s):  
Lauana Greicy Tonon Lemos ◽  
Gabriel Mello da Cunha Longo ◽  
Bruna dos Santos Mendonça ◽  
Marcela Cristina Robaina ◽  
Mariana Concentino Menezes Brum ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
3D Culture ◽  
3D Models ◽  
Mrna Levels ◽  
Antitumor Effects ◽  
Cell Growth And Migration ◽  
And Migration ◽  
2D And 3D

Drug resistance represents a major issue in treating breast cancer, despite the identification of novel therapeutic strategies, biomarkers, and subgroups. We have previously identified the LQB-223, 11a-N-Tosyl-5-deoxi-pterocarpan, as a promising compound in sensitizing doxorubicin-resistant breast cancer cells, with little toxicity to non-neoplastic cells. Here, we investigated the mechanisms underlying LQB-223 antitumor effects in 2D and 3D models of breast cancer. MCF-7 and MDA-MB-231 cells had migration and motility profile assessed by wound-healing and phagokinetic track motility assays, respectively. Cytotoxicity in 3D conformation was evaluated by measuring spheroid size and performing acid phosphatase and gelatin migration assays. Protein expression was analyzed by immunoblotting. Our results show that LQB-223, but not doxorubicin treatment, suppressed the migratory and motility capacity of breast cancer cells. In 3D conformation, LQB-223 remarkably decreased cell viability, as well as reduced 3D culture size and migration. Mechanistically, LQB-223-mediated anticancer effects involved decreased proteins levels of XIAP, c-IAP1, and Mcl-1 chemoresistance-related proteins, but not survivin. Survivin knockdown partially potentiated LQB-223-induced cytotoxicity. Additionally, cell treatment with LQB-223 resulted in changes in the mRNA levels of epithelial-mesenchymal transition markers, suggesting that it might modulate cell plasticity. Our data demonstrate that LQB-223 impairs 3D culture growth and migration in 2D and 3D models of breast cancer exhibiting different phenotypes.

Arsenic trioxide suppresses cell growth and migration via inhibition of miR-27a in breast cancer cells

2016 ◽  
Vol 469 (1) ◽  
pp. 55-61 ◽  
Author(s):  
Shunhua Zhang ◽  
Cong Ma ◽  
Haijie Pang ◽  
Fanpeng Zeng ◽  
Long Cheng ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Arsenic Trioxide ◽  
Breast Cancer Cells ◽  
Cell Growth And Migration ◽  
And Migration

scholarly journals Down-regulation of uPA and uPAR by 3,3′-diindolylmethane contributes to the inhibition of cell growth and migration of breast cancer cells

2009 ◽  
Vol 108 (4) ◽  
pp. 916-925 ◽  
Author(s):  
Aamir Ahmad ◽  
Dejuan Kong ◽  
Zhiwei Wang ◽  
Sanila H. Sarkar ◽  
Sanjeev Banerjee ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Down Regulation ◽  
Cell Growth And Migration ◽  
And Migration

HDAC1 triggers the proliferation and migration of breast cancer cells via upregulation of interleukin-8

2017 ◽  
Vol 398 (12) ◽  
pp. 1347-1356 ◽  
Author(s):  
Zhaohui Tang ◽  
Sijuan Ding ◽  
Honglin Huang ◽  
Pengfei Luo ◽  
Bohua Qing ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Nuclear Translocation ◽  
Interleukin 8 ◽  
Normal Fibroblast ◽  
Mrna Levels ◽  
Targeted Inhibition ◽  
And Migration ◽  
Proliferation And Migration

AbstractTargeted inhibition of histone deacetylase (HDAC) is one of the potent anticancer therapy approaches. Our data showed that mRNA and protein levels of HDAC1 in breast cancer cells were greater than that in normal fibroblast 3T3 cells and normal epithelial breast MCF10A cells. The mRNA levels of HDAC1 in 75% of breast cancer tissues (18/24) were greater than that in their corresponding adjacent normal tissues. Knockdown of HDAC1 by specific siRNAs can suppress the proliferation and migration of breast cancer cells and inhibit the expression of interleukin-8 (IL-8), while not IL-6. While recombinant IL-8 (rIL-8) can attenuate the suppression effects of si-HDAC1 on the proliferation and migration of breast cancer cells. HDAC1 can positively regulate the transcription and promoter activities of IL-8. While NF-κB and MAPK, two important signals responsible for the transcription of IL-8, did not mediate HDAC1 regulated IL-8 expression. The expression and nuclear translocation of Snail were increased in HDAC1 over expressed breast cancer cells. Targeted inhibition of Snail can attenuate HDAC1 over expression induced cell proliferation and migration. Collectively, our data showed that HDAC1 can trigger the proliferation and migration of breast cancer cells via activation of Snail/IL-8 signals.

scholarly journals Cyclophilin B as a co-regulator of prolactin-induced gene expression and function in breast cancer cells

2010 ◽  
Vol 44 (6) ◽  
pp. 319-329 ◽  
Author(s):  
Feng Fang ◽  
Jiamao Zheng ◽  
Traci L Galbaugh ◽  
Alyson A Fiorillo ◽  
Elizabeth E Hjort ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Cell Growth ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Breast Cancer Cells ◽  
Cell Growth And Migration ◽  
Cyclophilin B ◽  
And Migration

The effects of prolactin (PRL) during the pathogenesis of breast cancer are mediated in part though Stat5 activity enhanced by its interaction with its transcriptional inducer, the prolyl isomerase cyclophilin B (CypB). We have demonstrated that knockdown of CypB decreases cell growth, proliferation, and migration, and CypB expression is associated with malignant progression of breast cancer. In this study, we examined the effect of CypB knockdown on PRL signaling in breast cancer cells. CypB knockdown with two independent siRNAs was shown to impair PRL-induced reporter expression in breast cancer cell line. cDNA microarray analysis was performed on these cells to assess the effect of CypB reduction, and revealed a significant decrease in PRL-induced endogenous gene expression in two breast cancer cell lines. Parallel functional assays revealed corresponding alterations of both anchorage-independent cell growth and cell motility of breast cancer cells. Our results demonstrate that CypB expression levels significantly modulate PRL-induced function in breast cancer cells ultimately resulting in enhanced levels of PRL-responsive gene expression, cell growth, and migration. Given the increasingly appreciated role of PRL in the pathogenesis of breast cancer, the actions of CypB detailed here are of biological significance.

Effect of red laser irradiation and Ajwain essential oil on 2D and 3D culture models of MDA-MB-231 breast cancer cells

Biologia ◽  
2021 ◽  
Author(s):  
Elnaz Karimi ◽  
Zahra Kianmehr ◽  
Khatereh Khorsandi ◽  
Sepideh Zarie ◽  
Gholamreza Kavoosi
Keyword(s):  
Breast Cancer ◽  
Essential Oil ◽  
Cancer Cells ◽  
Laser Irradiation ◽  
Breast Cancer Cells ◽  
3D Culture ◽  
Culture Models ◽  
2D And 3D

scholarly journals Piperlongumine Induces Cell Cycle Arrest via Reactive Oxygen Species Accumulation and IKKβ Suppression in Human Breast Cancer Cells

Antioxidants ◽  
2019 ◽  
Vol 8 (11) ◽  
pp. 553 ◽  
Author(s):  
Chang Hee Jeong ◽  
Haram Ryu ◽  
Do Hyun Kim ◽  
Wei Nee Cheng ◽  
Jee Eun Yoon ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Mrna Levels ◽  
Cycle Arrest ◽  
Anticancer Effects ◽  
Er Positive ◽  
And Migration ◽  
Positive Breast Cancer

Piperlongumine (PL), a natural product derived from long pepper (Piper longum L.), is known to exhibit anticancer effects. However, the effect of PL on cell cycle-regulatory proteins in estrogen receptor (ER)-positive breast cancer cells is unclear. Therefore, we investigated whether PL can modulate the growth of ER-positive breast cancer cell line, MCF-7. We found that PL decreased MCF-7 cell proliferation and migration. Flow cytometric analysis demonstrated that PL induced G2/M phase cell cycle arrest. Moreover, PL significantly modulated the mRNA levels of cyclins B1 and D1, cyclin-dependent kinases 1, 4, and 6, and proliferating cell nuclear antigen. PL induced intracellular reactive oxygen species (hydrogen peroxide) accumulation and glutathione depletion. PL-mediated inhibition of IKKβ expression decreased nuclear translocation of NF-κB p65. Furthermore, PL significantly increased p21 mRNA levels. In conclusion, our data suggest that PL exerts anticancer effects in ER-positive breast cancer cells by inhibiting cell proliferation and migration via ROS accumulation and IKKβ suppression.

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