scholarly journals Overexpression of Galectin-7, A Myoepithelial Cell Marker, Enhances Spontaneous Metastasis of Breast Cancer Cells

2010 ◽  
Vol 176 (6) ◽  
pp. 3023-3031 ◽  
Author(s):  
Mélanie Demers ◽  
April A.N. Rose ◽  
Andrée-Anne Grosset ◽  
Katherine Biron-Pain ◽  
Louis Gaboury ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Myoepithelial Cell ◽  
Breast Cancer Cells ◽  
Cell Marker ◽  
Spontaneous Metastasis

Role of natural killer cells in hormone-independent rapid tumor formation and spontaneous metastasis of breast cancer cells in vivo

2006 ◽  
Vol 104 (3) ◽  
pp. 267-275 ◽  
Author(s):  
Md. Zahidunnabi Dewan ◽  
Hiroshi Terunuma ◽  
Masahiro Takada ◽  
Yuetsu Tanaka ◽  
Hiroyuki Abe ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Natural Killer Cells ◽  
Cancer Cells ◽  
Natural Killer ◽  
Breast Cancer Cells ◽  
Tumor Formation ◽  
Spontaneous Metastasis ◽  
Killer Cells

scholarly journals Intravascular Location of Breast Cancer Cells after Spontaneous Metastasis to the Lung

2002 ◽  
Vol 161 (3) ◽  
pp. 749-753 ◽  
Author(s):  
Christopher W. Wong ◽  
Chun Song ◽  
Maggie M. Grimes ◽  
Weili Fu ◽  
Mark W. Dewhirst ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Spontaneous Metastasis

scholarly journals Regulatory roles of lncRNA PANDAR in breast cancer cell proliferation

2021 ◽  
Vol 15 (6) ◽  
pp. 285-291
Author(s):  
Qinnuan Sun ◽  
Xiumei Wang
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Marker Gene ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Cell Marker ◽  
Mesenchymal Transition ◽  
Mcf 7

Abstract Background Breast cancer represents the second most deadly malignancy in women, and long noncoding RNAs (lncRNAs) have crucial functions in its development. Objective To investigate effects of the promoter of CDKN1A antisense DNA damage-activated RNA (PANDAR) on epithelial-mesenchymal transition (EMT) in breast cancer cells and their proliferation. Methods lncRNAs potentially regulating the transcriptional activity of the E-cadherin (E-cad, an epithelial cell marker) gene promoter were screened using a dual-luciferase reporter assay. PANDAR was overexpressed in Michigan cancer foundation 7 (MCF-7) breast cancer cells. E-cad and N-cadherin (N-cad, a mesenchymal cell marker) levels were detected by immunoblotting. Cell viability was assessed using a cell counting kit-8. Results PANDAR and TCONS00068220/LOC105375819 conservatively regulated the promoter activity of E-cad. PANDAR overexpression in MCF-7 inhibited E-cad expression, but upregulated N-cad. The enhanced expression of PANDAR promoted cell proliferation. Conclusion PANDAR is a key transcriptional repressor of E-cad and has regulatory effects on the promotion of cell proliferation. PANDAR is an oncogene in breast cancer, potentially facilitating the EMT process and promoting cell proliferation.

scholarly journals Knockdown of the prognostic cancer stem cell marker Musashi-1 decreases radio-resistance while enhancing apoptosis in hormone receptor-positive breast cancer cells via p21WAF1/CIP1

2021 ◽  
Author(s):  
Fabian M. Troschel ◽  
Heike Palenta ◽  
Katrin Borrmann ◽  
Kristin Heshe ◽  
San Hue Hua ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Stem Cell ◽  
Cancer Stem Cell ◽  
Cancer Cells ◽  
Prognostic Marker ◽  
Cancer Cell ◽  
Breast Cancer Cells ◽  
Stem Cell Marker ◽  
Cell Marker ◽  
Prognostic Relevance

Abstract Purpose While the stem cell marker Musashi-1 (MSI-1) has been identified as a key player in a wide array of malignancies, few findings exist on its prognostic relevance and relevance for cancer cell death and therapy resistance in breast cancer. Methods First, we determined prognostic relevance of MSI-1 in database analyses regarding multiple survival outcomes. To substantiate findings, MSI-1 was artificially downregulated in MCF-7 breast cancer cells and implications for cancer stem cell markers, cell apoptosis and apoptosis regulator p21, proliferation and radiation response were analyzed via flow cytometry and colony formation. Radiation-induced p21 expression changes were investigated using a dataset containing patient samples obtained before and after irradiation and own in vitro experiments. Results MSI-1 is a negative prognostic marker for disease-free and distant metastasis-free survival in breast cancer and tends to negatively influence overall survival. MSI-1 knockdown downregulated stem cell gene expression and proliferation, but increased p21 levels and apoptosis. Similar to the MSI-1 knockdown effect, p21 expression was strongly increased after irradiation and was expressed at even higher levels in MSI-1 knockdown cells after irradiation. Finally, combined use of MSI-1 silencing and irradiation reduced cancer cell survival. Conclusion MSI-1 is a prognostic marker in breast cancer. MSI-1 silencing downregulates proliferation while increasing apoptosis. The anti-proliferation mediator p21 was upregulated independently after both MSI-1 knockdown and irradiation and even more after both treatments combined, suggesting synergistic potential. Radio-sensitization effects after combining radiation and MSI-1 knockdown underline the potential of MSI-1 as a therapeutic target.

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