High expression of FBP1 and LDHB in fibroadenomas and invasive breast cancers

2021 ◽  
pp. 1-6
Author(s):  
Ika Yustisia ◽  
Rini Amriani ◽  
Husni Cangara ◽  
Syahrijuita Syahrijuita ◽  
A. Alfian Zainuddin ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Invasive Breast Cancer ◽  
Tumor Development ◽  
Staining Technique ◽  
High Expression ◽  
Breast Diseases ◽  
Breast Cancers ◽  
Embedded Blocks

BACKGROUND: The role of gluconeogenesis in cancer cells as the reverse pathway for glycolysis is not well known. Several studies of gluconeogenesis in cancer cells still show conflicting results. Expression of key enzymes such as FBP1 and LDHB in cancer tissues may explain the role of gluconeogenesis in tumor development. OBJECTIVE: This study aimed to analyze the expression of FBP1 and LDHB in fibroadenomas and invasive cancers of the breast. METHODS: The immunohistochemical staining technique was used to show the expression of FBP1 and LDHB in formalin-fixed, paraffin-embedded blocks of 32 fibroadenomas and 31 invasive breast cancer samples. RESULTS: FBP1 was expressed by the majority of fibroadenoma (68.7%) and invasive breast cancer (71%) samples. LDHB expression in fibroadenomas was significantly higher than in invasive breast cancers (P = 0.029). The expression of these two enzymes was found in lobular, ductal, and NST types of invasive breast cancers, and at low, intermediate, and high grades of malignancy. CONCLUSIONS: High expression of FBP1 and LDHB was found in fibroadenomas and invasive breast cancers. A higher level of LDHB expression was observed in fibroadenomas. These results may indicate the enzymes’ role in the pathogenesis of both breast diseases.

scholarly journals The Function Role of miR-181a in Chemosensitivity to Adriamycin by Targeting Bcl-2 in Low-Invasive Breast Cancer Cells

2013 ◽  
Vol 32 (5) ◽  
pp. 1225-1237 ◽  
Author(s):  
Ying Zhu ◽  
Jianzhong Wu ◽  
Shuchun Li ◽  
Rong Ma ◽  
Haixia Cao ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Invasive Breast Cancer ◽  
Breast Cancer Cells

scholarly journals Role of DNA methylation in miR-200c/141 cluster silencing in invasive breast cancer cells

2010 ◽  
Vol 3 (1) ◽  
Author(s):  
Rui Neves ◽  
Christina Scheel ◽  
Sandra Weinhold ◽  
Ellen Honisch ◽  
Katharina M Iwaniuk ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Dna Methylation ◽  
Cancer Cells ◽  
Invasive Breast Cancer ◽  
Breast Cancer Cells

scholarly journals The Long Non-Coding RNA SAMMSON Is a Regulator of Chemosensitivity and Metabolic Orientation in MCF-7 Doxorubicin-Resistant Breast Cancer Cells

Biology ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1156
Author(s):  
Charlotte Orre ◽  
Xavier Dieu ◽  
Jordan Guillon ◽  
Naïg Gueguen ◽  
Seyedeh Tayebeh Ahmadpour ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Metabolic Reprogramming ◽  
Breast Cancers ◽  
Rna Molecules ◽  
Non Coding Rna ◽  
Long Non Coding Rna ◽  
Mcf 7

Despite improvements in therapeutic strategies for treating breast cancers, tumor relapse and chemoresistance remain major issues in patient outcomes. Indeed, cancer cells display a metabolic plasticity allowing a quick adaptation to the tumoral microenvironment and to cellular stresses induced by chemotherapy. Recently, long non-coding RNA molecules (lncRNAs) have emerged as important regulators of cellular metabolic orientation. In the present study, we addressed the role of the long non-coding RNA molecule (lncRNA) SAMMSON on the metabolic reprogramming and chemoresistance of MCF-7 breast cancer cells resistant to doxorubicin (MCF-7dox). Our results showed an overexpression of SAMMSON in MCF-7dox compared to doxorubicin-sensitive cells (MCF-7). Silencing of SAMMSON expression by siRNA in MCF-7dox cells resulted in a metabolic rewiring with improvement of oxidative metabolism, decreased mitochondrial ROS production, increased mitochondrial replication, transcription and translation and an attenuation of chemoresistance. These results highlight the role of SAMMSON in the metabolic adaptations leading to the development of chemoresistance in breast cancer cells. Thus, targeting SAMMSON expression levels represents a promising therapeutic route to circumvent doxorubicin resistance in breast cancers.

scholarly journals BSCI-15. Osteopontin plays a crucial role in invasiveness of triple negative breast cancer cells in the context of human microglia

2021 ◽  
Vol 3 (Supplement_3) ◽  
pp. iii4-iii4
Author(s):  
Kamil Wojnicki ◽  
Agata Kochalska ◽  
Katarzyna Poleszak ◽  
Adria-Jaume Roura ◽  
Ewa Matyja ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Triple Negative Breast Cancer ◽  
Breast Cancer Cells ◽  
Triple Negative ◽  
Metastatic Breast ◽  
Breast Cancer Cell Lines ◽  
Breast Cancers ◽  
Human Microglia

Abstract The triple-negative breast cancer (TNBC) is the most malignant among breast cancers and has the high risk of developing metastasis into the brain. Metastases of breast cancers are increasing and pose a clinical challenge as the current treatments are not effective due to the unique brain microenvironment for metastatic breast cancer cells. While the contribution of brain macrophages to the formation of the metastatic niche is established, factors responsible for the crosstalk between cells remain elusive. SPP1 encoding a secreted phosphoprotein 1 (ostepontin) is highly overexpressed in malignant breast cancers. We evaluated the role of SPP1 in invasion and metastasis of human breast cancer cells. We found the increased invasion of triple-negative MDA-MB-231 (MDA-231) cells in the presence of human microglial HMSV40 cells. Using Western blot analysis demonstrated the elevated levels of focal adhesion kinase (FAK) and signal transducer and activator of transcription 3 (STAT3) in MDA-231 cells in co-cultures. Moreover, blocking SPP1 and integrin interactions with the synthetic RGD peptide, efficiently diminished both basic and microglia-induced invasion of MDA-231. To assess the role of SPP1 in cell invasion, we established the MDA-231 cells with knocked-down SPP1 expression using shRNA (shSPP1). Interestingly, the shSPP1 cells were unresponsive towards HMSV40 microglia. We have previously found that an antibiotic minocycline reduces SPP1 expression in glioma cells. We performed cell toxicity studies on 4 breast cancer cell lines and various non-malignant cells. All tested malignant cancer cells were more sensitize to minocycline than non-cancerous cells and breast cancer cells derived from TNBC were the most susceptible. Altogether, we demonstrate that microglia support invasion of breast cancer cells via SPP1/osteopontin triggering the integrin signalling, and minocycline by downregulating SPP1 expression may reduce both basic and microglia-induced cancer invasion. Therefore, we purpose that minocycline could be a new therapeutics targeting metastatic brain cancers.

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