scholarly journals The high expression of NUDT5 indicates poor prognosis of breast cancer by modulating AKT / Cyclin D signaling

PLoS ONE ◽  
2021 ◽  
Vol 16 (2) ◽  
pp. e0245876
Author(s):  
He Zhang ◽  
Li-Qun Zhang ◽  
Cheng-Cheng Yang ◽  
Jin Li ◽  
Xin-Yuan Tian ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Breast Tumor ◽  
Poor Prognosis ◽  
High Expression ◽  
Breast Cancer Cell Lines ◽  
Cyclin D ◽  
Tumor Tissues

NUDIX hydrolase type 5 (NUDT5) is a kind of ADP-ribose pyrophosphatase and nucleotide metabolizing enzyme in cell metabolism. Previous studies have shown NUDT5 expression affected chromosome remodeling, involved in cell adhesion, cancer stem cell maintenance and epithelial to mesenchyme transition in breast cancer cells. Nevertheless, the role of NUDT5 in breast cancer progression and prognosis has not yet been systematically studied. This study explored the association of NUDT5 with the tumor development and poor prognosis in patients with breast cancer. Our results show that the levels of NUDT5 were upregulated in breast cancer cell lines and breast tumor tissues, and the expression of NUDT5 in breast tumor tissues increased significantly when compared with adjacent non-tumorous tissues by immunohistochemical staining of tissue microarrays. Breast cancer patients with high NUDT5 expression had a worse prognosis than those with low expression of NUDT5. In addition, the knockdown of NUDT5 suppressed breast cancer cell lines proliferation, migration and invasion, and dramatically inhibited the AKT phosphorylation at Thr308 and expression of Cyclin D1. The opposite effects were observed in vitro following NUDT5 rescue. Our findings indicated that the high expression of NUDT5 is probably involved in the poor prognosis of breast cancer via the activation of the AKT / Cyclin D pathways, which could be a prognostic factor and potential target in the diagnosis and treatment of breast cancer.

scholarly journals Productive Infection of Human Breast Cancer Cell Lines with Human Cytomegalovirus (HCMV)

Pathogens ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 641
Author(s):  
Kaitlin M. Branch ◽  
Erica C. Garcia ◽  
Yin Maggie Chen ◽  
Matthew McGregor ◽  
Mikayla Min ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Breast Tumor ◽  
Cancer Cell Lines ◽  
Breast Cancer Cell Lines ◽  
Human Breast ◽  
Breast Tumor Cells

Breast cancer is the leading cause of cancer deaths among women worldwide. There are many known risk factors for breast cancer, but the role of infectious disease remains unclear. Human cytomegalovirus (HCMV) is a widespread herpesvirus that usually causes little disease. Because HCMV has been detected in breast tumor biopsy samples and is frequently transmitted via human breast milk, we investigated HCMV replication in breast tumor cells. Four human breast cancer cell lines with different expression profiles for the key diagnostic markers of the estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2), were infected with a bacterial artificial chromosome-derived HCMV clinical strain TB40/E tagged with green fluorescent protein (GFP). Fluorescence microscopy confirmed that all four breast cancer cell lines supported virus entry. RNA was isolated from infected cells and the expression of immediate early (UL123), early (UL54), and late (UL111A) genes was confirmed using PCR. Viral proteins were detected by immunoblotting, and viral progeny were produced during the infection of breast tumor cells, as evidenced by subsequent infection of fibroblasts with culture supernatants. These results demonstrate that breast tumor cells support productive HCMV infection and could indicate that HCMV replication may play a role in breast cancer progression.

scholarly journals CD146 expression is associated with a poor prognosis in human breast tumors and with enhanced motility in breast cancer cell lines

2009 ◽  
Vol 11 (1) ◽  
Author(s):  
Gwladys Zabouo ◽  
Anne-Marie Imbert ◽  
Jocelyne Jacquemier ◽  
Pascal Finetti ◽  
Thomas Moreau ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Poor Prognosis ◽  
Breast Tumors ◽  
Cancer Cell Lines ◽  
Breast Cancer Cell Lines ◽  
Human Breast ◽  
Cd146 Expression

scholarly journals IQGAP3 Overexpression Correlates With Poor Prognosis and Radiation Therapy Resistance in Breast Cancer

2021 ◽  
Vol 11 ◽  
Author(s):  
Xin Hua ◽  
Zhi-Qing Long ◽  
Ling Guo ◽  
Wen Wen ◽  
Xin Huang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Radiation Therapy ◽  
Cancer Patients ◽  
Cell Lines ◽  
Breast Cancer Cell ◽  
Subgroup Analysis ◽  
Poor Prognosis ◽  
Breast Cancer Cell Lines ◽  
Breast Cancer Patients ◽  
Tumor Tissues

Background: IQ motif-containing GTPase activating protein 3 (IQGAP3), the latest identified member of the IQGAP family, may act as a crucial factor in cancer development and progression; however, its clinical value in breast cancer remains unestablished. We explored the correlation between IQGAP3 expression profile and the clinicopathological features in breast cancer.Methods: IQGAP3 mRNA and protein levels were detected in breast cancer cell lines and tumor tissues by real-time PCR and western blotting and compared to the normal control groups. Protein expression of IQGAP3 was also evaluated immunohistochemically in archived paraffin-embedded specimens from 257 breast cancer patients, and the associations between IQGAP3 expression level, clinical characteristics, and prognosis were analyzed. We assessed the relationship between IQGAP3 expression and sensitivity to radiation therapy which was determined by subgroup analysis.Results: IQGAP3 was significantly upregulated in breast cancer cell lines and human tumor tissues at both the mRNA and protein level compared to controls. Additionally, high levels of IQGAP3 expression were detected in 110/257 (42.8%) of archived paraffin-embedded breast cancer specimens. High IQGAP3 expression level was significantly related to clinical stage (p = 0.001), T category (p = 0.002), N category (p = 0.001), locoregional recurrence (p = 0.002), distant metastasis (p = 0.001), and vital status (p = 0.001). Univariate and multivariate statistical analysis showed that IQGAP3 expression was an independent prognostic factor among all 257 breast cancer patients in our cohort (p = 0.003, p = 0.001). Subgroup analysis revealed IQGAP3 expression correlated with radioresistance and was also an independent predictor of radiotherapy outcome.Conclusion: Our findings suggest that high IQGAP3 expression predicts poor prognosis and radioresistance in breast cancer. Therefore, IQGAP3 may be a reliable prognostic biomarker in breast cancer and could be used to identify patients who may benefit from radiotherapy.

scholarly journals HER2/neu Oncogene and Sensitivity to the DNA-Interactive Drug Doxorubicin

2020 ◽  
Vol 4 (1) ◽  
Author(s):  
Anne Mullin ◽  
Bertrand Jean-Claude
Keyword(s):  
Breast Cancer ◽  
Dna Binding ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Breast Tumor ◽  
Cancer Cell Lines ◽  
Chemotherapeutic Agents ◽  
Breast Cancer Cell Lines ◽  
Protein Levels

Breast tumor cells overexpressing the proto-oncogene HER2/neu are known to be less responsive to certain DNA-binding chemotherapeutic agents. The current study specifically investigates the correlation between chemosensitivity to the DNA-binding drug doxorubicin and cellular HER2/neu protein levels in a panel of eight breast cancer cell lines (HS-578, BT-474, MDA-MB-453, MDA-MB-231, MDA-MB-175, MCF-7, ZR-75-1 and T47D). The IC50 (the drug concentration required to inhibit cell growth by 50%) values for the cell lines were determined by the sulforhodamine B assay. IC50 values were correlated with HER2/neu protein levels determined by Western blotting. An almost linear relationship between IC50 and HER2/neu protein level for seven cell lines (p = 0.02, r2 = 0.680) was found, with protein levels increasing as resistance increased. The findings suggest that overexpression of HER2/neu correlates with increased resistance to doxorubicin in seven of eight breast cancer cell lines studied. The observation that, in one cell line (MDA-MB-175), doxorubicin IC50 did not correlate with HER2/neu levels, suggests that in these cells, an as-of-yet unidentified factor contributes to resistance. If the observed correlation, which was present in seven of eight cell lines, is confirmed in a larger sample size, increased HER2/neu levels may be implemented as a predictor of breast tumor sensitivity to doxorubicin.

scholarly journals Activator Protein-2β Promotes Tumor Growth and Predicts Poor Prognosis in Breast Cancer

2018 ◽  
Vol 47 (5) ◽  
pp. 1925-1935 ◽  
Author(s):  
Zhenglin Li ◽  
Xiangdong Xu ◽  
Meihua Luo ◽  
Jiaojiao Hao ◽  
Shilei Zhao ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Growth ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Colony Formation ◽  
Poor Prognosis ◽  
Breast Cancer Cells ◽  
Breast Cancer Cell Lines

Background/Aims: Activator protein-2 (AP-2) transcription factors have been proved to be essential in maintaining cellular homeostasis and regulating the transformation from normal growth to neoplasia. However, the role of AP-2β, a key member of AP-2 family, in breast cancer is rarely reported. Methods: The effect of AP-2 on cell growth, migration and invasion in breast cancer cells were measured by MTT, colony formation, wound-healing and transwell assays, respectively. The expression levels of AP-2β and other specific markers in breast cancer cell lines and tissue microarrays from the patients were detected using RT-PCR, Western blot and immunohistochemical staining. The regulation of AP-2β on tumor growth in vivo was analyzed in a mouse xenograft model. Results: We demonstrated the tumor-promoting function of AP-2β in breast cancer. AP-2β was found to be highly expressed in breast cancer cell lines and tumor tissues of breast cancer patients. The shRNA-mediated silencing of AP-2β led to the dramatic inhibition of cell proliferation, colony formation ability, migration and invasiveness in breast cancer cells accompanied by the down-regulated expression of some key proteins involved in cancer progression, including p75, MMP-2, MMP-9, C-Jun, p-ERK and STAT3. Overexpression of AP-2β markedly up-regulated the levels of these proteins. Consistent with the in vitro study, the silencing or overexpression of AP-2β blocked or promoted tumor growth in the mice with xenografts of breast cancers. Notably, the high AP-2β expression levels was correlated with poor prognosis and advanced malignancy in patients with breast cancer. Conclusions: Our study demonstrates that AP-2β promotes tumor growth and predicts poor prognosis, and may represent a potential therapeutic target for breast cancer.

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