mcf-7   31

Hypoxia promotes breast cancer cell invasion through HIF-1α-mediated up-regulation of the invadopodial actin bundling protein CSRP2 | Scientific Reports
Interesting that hypoxia stimulates IPs in 231 and 4T1. MCF7 make precursors but they say do not express MMP14 and thus matrix degradation is low in MCF7

Hypoxia is a common feature of solid tumours that promotes invasion and metastatic dissemination. Invadopodia are actin-rich membrane protrusions that direct extracellular matrix proteolysis and facilitate tumour cell invasion. Here, we show that CSRP2, an invadopodial actin bundling protein, is upregulated by hypoxia in various breast cancer cell lines, as well as in pre-clinical and clinical breast tumour specimens. We functionally characterized two hypoxia responsive elements within the proximal promoter of CSRP2 gene which are targeted by hypoxia-inducible factor-1 (HIF-1) and required for promoter transactivation in response to hypoxia. Remarkably, CSRP2 knockdown significantly inhibits hypoxia-stimulated invadopodium formation, ECM degradation and invasion in MDA-MB-231 cells, while CSRP2 forced expression was sufficient to enhance the invasive capacity of HIF-1α-depleted cells under hypoxia. In MCF-7 cells, CSRP2 upregulation was required for hypoxia-induced formation of invadopodium precursors that were unable to promote ECM degradation. Collectively, our data support that CSRP2 is a novel and direct cytoskeletal target of HIF-1 which facilitates hypoxia-induced breast cancer cell invasion by promoting invadopodia formation.
invadopodium  MCF-7  231_cells  4t1  hypoxia 
11 days ago by Segalllab
Inhibition of Notch signaling pathway enhanced the radiosensitivity of breast cancer cells - Peng - 2018 - Journal of Cellular Biochemistry - Wiley Online Library
4Gy induced NOTCH1 protein and activation in MCF7/T47D as well as invasion. No analysis of ligands. Possibly look at radiation effects on macrophages?

This study aimed to investigate the effect of inhibiting the Notch signaling pathway on the radiosensitivity of breast cancer cells. Human breast cancer cell lines (MCF‐7 and T47D) were selected and treated with radiation of different doses. Cells were treated with Gamma secretase inhibitor (GSI) to analyze the effects of GSI on the Notch signaling, which were detected by Immunofluorescence assay, RT‐qPCR, and Western blot analysis. Besides, Transwell assay, Scratch test, colony formation assay, MTT assay, and flow cytometry were conducted to show the effects of GSI on the invasion and migration, survival fraction, cell viability, and apoptosis of MCF‐7 and T47D cells after radiation therapy. Moreover, cell transfection with a dominant negative mutant of RBPJ, the key transcription factor of Notch signaling pathway, were also applied to show the inhibition of Notch signaling pathway. Initially, we found that the 4 Gy radiation activated Notch signaling pathway, and enhanced the invasion and migration of MCF‐7 and T47D cells. However, GSI inhibited the Notch signaling pathway, and reversed the enhancement of radiation on the migration and invasion, promoted the enhancement of apoptosis and inhibition of proliferation of MCF‐7 and T47D cells induced by radiation. Except that, we also determined that GSI and dnRBPJ suppressed the upregulation of Notch signaling after radiation therapy. Our study demonstrated that inhibition of the Notch signaling pathway enhanced the radiosensitivity of breast cancer cells, which may provide evident for a beneficial adjuvant therapy in the breast cancer treatment.
Notch  radiation  radiosensitivity  MCF-7  T47D  GSI  invasion 
5 weeks ago by Segalllab
Macrophage inflammatory factors promote epithelial-mesenchymal transition in breast cancer
Claim the TPA stimulated THP1s are M1 phenotype - stimulates MCF7 and T47D partial EMT. Jan Geliebter at Valhalla

"Previous studies have demonstrated that human monocytic cell lines such as THP-1 when activated with TPA exhibit an M1 phenotype [32–34]. We generated CM and observed that following the activation of THP-1 with TPA, there was enhanced expression of M1 marker iNOS in addition to pro-inflammatory cytokines IL-6, TNF-α, IL-1β, and IL-8 when compared to unactivated THP-1.
THP-1  macrophage_polarization  M1_macrophages  partial_emt  MCF-7  T47D 
11 weeks ago by Segalllab
Interference of Notch 1 inhibits the proliferation and invasion of breast cancer cells: Involvement of the β‑catenin signaling pathway
role for notch in 231 and mcf7 invasion

Breast cancer is one of the most common types of carcinoma in humans. The aim of the present study was to identify the role of Notch 1 in the proliferation and invasion of human breast cancer cells. Firstly, the levels of Notch 1 were determined by western blot analysis in breast cancer cell lines, and the results revealed that the expression levels of Notch 1 were markedly higher in MDA‑MB‑231 and MCF‑7 cells, and lower in MCF‑10A cells, compared with human mammary epithelial cells. An MTT assay was used to determine the viability of breast cancer cells. The optical density (OD)490 values were significantly decreased in Notch 1 short hairpin (sh)RNA‑transfected MCF‑7 and MDA‑MB‑231 cells, compared with the OD490 values in the negative control shRNA‑transfected cells. The MCF‑7 cells and MDA‑MB‑231 cells were also treated with increasing concentrations of MRK003, a Notch 1 inhibitor, for 24, 48 and 72 h, respectively. The inhibition rate was gradually increased in the MRK003‑treated cells in a time‑ and dose‑dependent manner. The invasive ability of the cells was determined using a Transwell migration assay. The migration ability was significantly decreased in the Notch 1‑transfected MCF‑7 cells and MDA‑MB‑231 cells. The molecular mechanism was examined, and the knockdown of Notch 1 significantly decreased the expression levels of β‑catenin, matrix metalloproteinase (MMP)‑2 and MMP‑9, and was also correlated with the downregulation of β‑catenin in the nucleus. In conclusion, Notch 1 was key in the progression of breast cancer, and knocking down the expression of Notch 1 significantly suppressed the proliferation and invasion of breast cancer cells. This provides novel clues for cancer therapy in human breast cancer.
Notch  invasion  231  MCF-7 
april 2018 by Segalllab
Regulation of the prometastatic neuregulin–MMP13 axis by SRC family kinases: therapeutic implications - Orive-Ramos - 2017 - Molecular Oncology - Wiley Online Library
Was for MCF7. Might be interesting to see if SFKs are important for macrophages. MMP13 was not induced in Ramon's data.

"ere, we show that dasatinib restricted NRG-induced MMP13 upregulation, both in vitro and in vivo, and in vivo metastatic dissemination of breast cancer cells. Chemical proteomics studies showed that the main cellular targets of dasatinib were SRC family kinases (SFKs). Moreover, genetic studies showed that knockdown of SRC or YES strongly inhibited NRG-induced MMP13 upregulation in vitro. Mechanistically, dasatinib treatment or knockdown of SRC also inhibited ERK1/2 kinases in vitro, which were required for NRG-induced MMP13 upregulation. These results open the possibility of clinically exploring the antitumoral action of dasatinib in those tumors in which the NRG–MMP13 signaling axis may play a relevant role in the control of tumor cell dissemination."
MCF-7  NRG1  mmp13  src  src_family_kinases 
february 2018 by Segalllab
Inhibitory Effects of Activin on the Growth and Morphogenesis of Primary and Transformed Mammary Epithelial Cells
Activin Ba and activin type II receptor is expressed by basal cells (by qPCR), and inhibits growth of MCF7 cells.
activin  myoepithelial_cells  luminal_cells  MCF-7 
january 2018 by Segalllab
Notch1 signaling regulates the epithelial–mesenchymal transition and invasion of breast cancer in a Slug-dependent manner
using immobilized jag1, examine various notch receptors and effects on emt and motility/invasion in 231 and mcf7 cells
Notch  JAG1  231_cells  MCF-7  EMT  migration  invasion 
september 2017 by Segalllab
Single factors alone can induce mesenchymal-like morphology, but not promote full EMT in breast cancer cell lines with different hormone statuses
hmm - a bit confusing - jag1 and hypoxia can induce morphological changes in mcf7 but not a clear EMT by western markers, and has less of an effect on BT474. They actually do some hypoxia studies with BT549 but not in response to JAG1
JAG1  MCF-7  BT474  BT549  EMT  hypoxia 
july 2017 by Segalllab
Jagged1 promotes aromatase inhibitor resistance by modulating tumor-associated macrophage differentiation in breast cancer patients | SpringerLink
correlation between jag1 expression (probably on tumor cells?) vs endocrine resistance in human cancers and then indication that coculture of mcf7 with thp1 can induce tam-like features in a possibly notch dependent way. They focus on how tumor cell jag1 can possibly induce M2/TAM properties in macrophages.
Macrophage  MCF-7  THP-1  JAG1  Notch  drug_resistance  tamoxifen_resistance  TAMs 
july 2017 by Segalllab
Targeted inhibition of Notch1 gene enhances the killing effects of paclitaxel on triple negative breast cancer cells
basically just that KD of notch enhances taxol induced killing. Would be interesting to see if macrophages stimulate resistance to taxol in a notch dependent way.
231_cells  MCF-7  paclitaxel-resistance  notch 
june 2017 by Segalllab
Induction of LIFR confers a dormancy phenotype in breast cancer cells disseminated to the bone marrow : Nature Cell Biology : Nature Research
lifr signaling may maintain dormancy, especially in bone marrow, and loss of lifr signaling can stimulate proliferation there.
lifr  dormancy  bone_marrow  metastasis  MCF-7  SUM159 
january 2017 by Segalllab
Macrophage phenotypic subtypes diametrically regulate epithelial-mesenchymal plasticity in breast cancer cells | BMC Cancer | Full Text
Use THP1 differentiation into M1 or M2 and coculture with MCF7 or 231 cells. M2 induces some EMT in MCF7 while M1 induce someMET in 231 cells.
THP-1  MCF-7  231_cells  macrophage_polarization  EMT  MET 
october 2016 by Segalllab
Three-Dimensional Breast Cancer Models Mimic Hallmarks of Size-Induced Tumor Progression | Cancer Research
made different size tumor aggregates and show tha tMCF7 and T47D can become more aggressive in large aggregates, in part through hypoxia, and that this may remain for a while after placement into smaller aggregates. Could be that we should precondition ER positive cells in aggregates before testing them?
MCF-7  T47D  spheroid  hypoxia  EMT  invasion  collective_migration 
october 2016 by Segalllab
Oncogene - Breast cancer dissemination promoted by a neuregulin-collagenase 3 signalling node
Patient IHC study showing that tumors with increased NRG1 have worse outcome. Also studies of invasion of MCF7 induced by NRG1
nrg1  prognosis  MCF-7  invasion 
august 2016 by Segalllab
Molecular Therapy - Inhibiting Notch Activity in Breast Cancer Stem Cells by Glucose Functionalized Nanoparticles Carrying [gamma]-secretase Inhibitors
interesting idea that notch induced csc's have increased glycolysis and they target that through linking glucose to nanoparticles containing dapt. Unfortunately they do not have a key control (glucose nanoparticles without dapt) to determine the importance of the notch targeting.
notch  dapt  231_cells  MCF-7  cancer  stem  cells  glycolysis 
june 2016 by Segalllab
Cyclooxygenase-2 in tumor-associated macrophages promotes breast cancer cell survival by triggering a positive-feedback loop between macrophages and cancer cells
Shows a feedback loop between TAMs and Tumor cells where COX2 positive TAMs increase tumor cell survival and proliferation, as well as induce COX2 expression in tumor cells. This tumor cell COX2 polarizes TAMs towards M2, and maintains a COX2+ population of TAMs.
MDA-MB  231  MCF-7  TAM  M2  COX2  Bcl-2  P-gp  Bax 
september 2015 by Segalllab
Human breast cancer cells educate macrophages toward the M2 activation status
Culturing PBMCs with conditioned media from MDA-MB 231 cells polarizes them to a more M2-like phenotype. They saw increased production of IL-6, IL-8, IL-10 and MMP-9.
MDA-MB  231  TAM  PBMC  MCF-7  T47D  cd163  M-CSF  CSF1 
august 2015 by Segalllab
IJMS | Free Full-Text | Exposure of Tumor-Associated Macrophages to Apoptotic MCF-7 Cells Promotes Breast Cancer Growth and Metastasis
Growth of MCF-7 cells in conditioned media from a Macrophage/Apoptotic MCF7 co-culture increases the CD44+/CD24- proportion of cancer stem cells, as well as increases metastasis to the liver and the lungs. Gene expression of the co-cultured macrophages show an upregulation of IL-6 mRNA. They propose that their results could possibly be due to increased IL-6 secretion by macrophages, leading to increased STAT3 signaling in tumor cells.
MCF-7  macrophage  apoptosis  co-culture  CD44  CD24  IL-6  STAT3 
june 2015 by Segalllab

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