Sentences with phrase «cycling hypoxia»

ESA staining of MDA - MB 231 (total cell population) and MDA - MB 231 F3 (cycling hypoxia - selected subpopulation) cells is shown.

Furthermore, the cycling hypoxia - selected F3 subpopulations had increased mRNA levels of three mesenchymal transcription factors - Snail (7 - to 10-fold), Slug (2 - to 3-fold), and Twist (2 - to 4-fold)- as measured by qRT - PCR (Figure 6d).

With the recent success of identifying selective inhibitors targeting CSCs, we believe that the newly isolated cycling hypoxia - selected subpopulation may present a new opportunity for chemical screening and discovery of compounds with selective toxicity for metastatic breast CSCs.

Furthermore, we found that the stem - like and EMT phenotypes observed in the cycling hypoxia - selected subpopulation are not reversible, because we obtained the same molecular profile from this subpopulation by culturing them as spherical cultures for several months in normal oxygen content and culturing them as adherent cells (Figure S2 in Additional file 2).

ESA staining of MDA - MB 231 (total cell population) and MDA - MB 231 F3 (cycling hypoxia - selected subpopulation) cells.

The colony formation and proliferation of the parent cell lines and the cycling hypoxia - selected subpopulations.

The Student t test was used to calculate the significance of increased CD44 + / CD24 - / ESA + and E-cad - / CD44 + / CD24 - populations in the cycling hypoxia - selected subpopulations.

Expression of epithelial - mesenchymal transition (EMT)- associated markers in the total cell population and the cycling hypoxia - selected subpopulation.

Therefore, we speculated that molecular machinery found to promote EMT might also be upregulated in the cycling hypoxia - selected subpopulation.

The percentage of CSCs in the cycling hypoxia selected subpopulation was analyzed based on the CD44, CD24, ESA, and E-cadherin expression by three - color flow cytometry.

We are currently exploring this possibility and hope to elucidate the mechanism and relevance of the cycling hypoxia - selected cell population in breast cancer progression.

Also, as shown in our study, the surviving cycling hypoxia - selected subpopulation acquires additional molecular advantages after exposure to several cycles of hypoxia / reoxygenation.

Growth curves of primary tumors generated from the parental cell lines and cycling hypoxia - selected subpopulations.

Therefore, downregulation of miR - 215 could promote EMT phenotype in downregulation of E-cadherin and promote EMT phenotype in the cycling hypoxia - selected subpopulation.

(b) The same flow cytometry analysis for BCM2 (total cell population) and BCM2 F3 (cycling hypoxia - selected subpopulation) cells.

(c) Proliferation curves of the parental cells, hypoxia - exposed cells (A3), and the cycling hypoxia - selected subpopulations grown as adherent cultures (top two plots) or as spherical cultures (the third plot).

In addition to miRNA200c and miR205, the cycling hypoxia - selected subpopulation showed decreased miR215 expression (Figure 6e).

Together, our results reinforce the idea that EMT and stem cell factors work cooperatively in highly tumorigenic cancer subpopulations and raise interesting questions about their contribution to the increased metastatic capability observed in the cycling hypoxia - selected subpopulation.

Limiting dilution tumor formation of parental, hypoxia - exposed adherent, and cycling hypoxia - selected breast cancer cells in vivo

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Here, we show that a non-adherent, stem - like, and metastatic CSC - enriched subpopulation could be isolated by exposing human metastatic breast cancer cell lines to cycles of chronic hypoxia followed by reoxygenation.

In our study, we found that exposing metastatic breast cancer cell lines to hypoxia and reoxygenation cycles induces a unique subpopulation that is highly metastatic and exhibits stem - like and EMT phenotypes.

These findings strongly suggest that we have succeeded in isolating a unique metastatic CSC population by exposing breast cancer cells to repetitive cycles of hypoxia and reoxygenation.

Therefore, we hypothesize that hypoxia / reoxygenation cycles may provide the driving force to select for a highly metastatic breast CSC subpopulation.

We then isolated and exposed this novel subpopulation to additional cycles of hypoxia / reoxygenation and established a distinct subpopulation of cells from these two breast cancer cell lines.

In our study, we found that the emergence of a small non-adherent subpopulation (approximately 1 %) survived after the first hypoxia / reoxygenation cycle and speculate that cyclic exposures of hypoxia and reoxygenation may select for the stem - like subpopulation with the ability to overcome replication arrest whereas the majority of non-adherent cells can not.

To study the effect of hypoxia / reoxygenation cycles on breast cancer, we exposed two metastatic human breast cancer cell lines (MDA - MB 231 and BCM2) to cycles of chronic hypoxia and nutrient deprivation.

Specifically, the way in which carbohydrate metabolism is affected, with severe deactivation of the tricarboxylic acid cycle, while glycolysis is activated (FDR < 10 − 27; Fig. 6d, Supplementary Table 9), suggests that hypoxia is likely playing a major role in the initial pre - to post-mortem transition (FDR 7.2 × 10 − 67).

Conditions for hypoxia / reoxygenation cycles were optimized using two human metastatic breast cancer cell lines (MDA - MB 231 and BCM2).

In response to cellular stress such as DNA damage, oncogene activation, transcriptional inhibition, and hypoxia, tumor suppressor p53 is activated and expressed, and acts as a transcription factor to induce its target genes [1], thereby playing a central role in the regulation of DNA repair, cell cycle, apoptosis, senescence, and angiogenesis [2 - 4].

Expression of hypoxia - inducible factor - 1alpha and cell cycle proteins in invasive breast cancer are estrogen receptor related

That response was even better during certain stages of the menstrual cycle in younger female rats, suggesting female hormones play a role in the response to hypoxia during sleep.