Basaloides Plattenepithelkarzinom (basaloid-squamöses Karzinom) des Mundbodens

Strassburger, Silke; Hyckel, Peter; Schumann, D.; Berndt, Alexander; Kosmehl, Hartwig

doi:10.1007/bf03043557

Cited by 3 publications

(2 citation statements)

References 15 publications

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“…The HER-2/neu-over-expressing breast carcinoma cell line SK-BR-3 [10] (Deutsches Krebsforschungszentrum Heidelberg, Germany) and the normal-expressing basaloid squamous cell carcinoma cell line PE/CA-PJ34 (ECACC No. 97062513, [11,12]) were cultured in Dulbecco's Minimal Essential Medium (DMEM, Gibco Karlsruhe, Germany) containing 10% fetal calf serum (Gibco Karlsruhe, Germany) and incubated in a humidified incubator at 37°C with 5% CO 2 . "Normal-expressing cells" means that the HER-2/neu protein has-like other tumour markers-a ubiquitous baseline expression and that it is not exclusively expressed in certain cell types.…”

Section: Methodsmentioning

confidence: 99%

Near-infrared fluorescence imaging of HER-2 protein over-expression in tumour cells

et al. 2004

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The aim of this study was to evaluate in vitro and in vivo imaging of HER-2-over-expressing tumours using near-infrared optical imaging. A fluorochrome probe was designed by coupling Cy5.5 to anti-HER-2 antibodies. Cells over-expressing (SK-BR-3 cells) or normally expressing (PE/CA-PJ34 cells) the HER-2 protein were incubated with the probe. After removing unbound probe molecules, fluorescence intensities were determined (a.u.: arbitrary units). Cells were additionally investigated using FACS and laser scanning microscopy. The probe was also injected intravenously into tumours bearing SK-BR-3 ( n=3) or PE/CA-PJ34 ( n=3). Whole-body fluorescence images were generated and analysed. The incubation of SK-BR-3 cells with the probe led to higher fluorescence intensities [2,133 (+/-143) a.u.] compared to controls [975 (+/-95) a.u.]. The results from FACS and immunocytochemical analysis were in agreement with these findings. A distinct dependency between the fluorescence intensity and the cell number used in the incubations was detected. In vivo, the relative fluorescence intensities in SK-BR-3 tumours were higher than in PE/CA-PJ34 tumours at 16-24 h after probe application. HER-2-over-expressing tumours were depictable in their original size. Labelling of HER-2 with Cy5.5 is suitable for in vitro and in vivo detection of HER-2-over-expressing tumour cells.

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Section: Methodsmentioning

confidence: 99%

Near-infrared fluorescence imaging of HER-2 protein over-expression in tumour cells

et al. 2004

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“…It is commonly regarded as triple-negative breast cancer, which is defined as lacking estrogen receptor, progesterone receptor and human epidermal growth factor receptor 2. Because of highly heterogeneous and many molecular subtypes, triple-negative breast cancer is difficult to treat [ 3 – 8 ].…”

Section: Introductionmentioning

confidence: 99%

Downregulation of TBC1 Domain Family Member 24 (BC1D24) Inhibits Breast Carcinoma Growth via IGF1R/PI3K/AKT Pathway

Zhao

et al. 2018

Med Sci Monit

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BackgroundTBC1 domain family member 24 (TBC1D24) pathogenic mutations affect its binding to ARF6 and then result in severe impairment of neuronal development. However, there are no reports about the expression and function of TBC1D24 in cancer. The aim of the present study was to evaluate the effect of proliferation, migration, and invasion after silencing TBC1D24 expression in breast cancer MCF-7 cells, and to elucidate the potential mechanism of TBC1D24 in breast cancer.Material/MethodsThe expression of TBC1D24 in breast cancer tissues and the adjacent non-tumor tissues was determined by S-P immunohistochemistry. The malignant behavior, including proliferation, migration, and invasion ability, was determined after silencing TBC1D24 in breast cancer MCF-7 cells. The expression of IGF1R was determined after silencing TBC1D24. The expression of TBC1D24 and IGF1R was detected after transfecting miR-30a mimics or inhibitors. The effect of TBC1D24 on MCF-7 cells growth in vivo was evaluated by a tumor xenograft study.ResultsTBC1D24 expression was elevated and was associated with poor outcome in breast carcinoma. TBC1D24 high expression was significantly correlated with unfavorable OS and RFS for breast cancer patients (p<0.05). Silencing TBC1D24 inhibited the proliferation, migration, and invasion ability of MCF-7 cells. TBC1D24 and IGF1R expression were decreased when transfected with miR-30a mimics. However, TBC1D24 and IGF1R expression were increased when transfected with miR-30a inhibitors (p<0.05). Knockdown of TBC1D24 inhibited the expression of IGF1R, PI3K, and p-AKT (p<0.05). Knockdown of TBC1D24 abolished tumorigenicity of MCF-7 cells. The average volume and weight of tumors was lower after silencing TBC1D24 expression (P<0.05).ConclusionsSilencing TBC1D24 inhibited MCF-7 cells growth in vitro and in vivo. TBC1D24 promoted breast carcinoma growth through the IGF1R/PI3K/AKT pathway. TBC1D24 is a potential therapeutic target for breast cancer.

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Orale Karzinome

Seifert¹

2000

Oralpathologie

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Basaloides Plattenepithelkarzinom (basaloid-squamöses Karzinom) des Mundbodens

Cited by 3 publications

References 15 publications

Near-infrared fluorescence imaging of HER-2 protein over-expression in tumour cells

Near-infrared fluorescence imaging of HER-2 protein over-expression in tumour cells

Downregulation of TBC1 Domain Family Member 24 (BC1D24) Inhibits Breast Carcinoma Growth via IGF1R/PI3K/AKT Pathway

Orale Karzinome

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