scholarly journals Secretion of BMP-2 by tumor-associated macrophages (TAM) promotes microcalcifications in breast cancer

BMC Cancer ◽  
2022 ◽  
Vol 22 (1) ◽  
Author(s):  
Shuo Wang ◽  
Haiyang Jiang ◽  
Caiwei Zheng ◽  
Ming Gu ◽  
Xinyu Zheng
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Immunohistochemical Staining ◽  
Breast Cancer Cells ◽  
Immunohistochemical Analysis ◽  
Bone Morphogenetic Protein 2 ◽  
Tumor Associated Macrophages ◽  
Alizarin Red ◽  
Underlying Mechanisms ◽  
Mcf 7

Abstract Introduction Breast microcalcifications is a characteristic feature in diagnostic imaging and a prognostic factor of breast cancer. However, the underlying mechanisms of breast microcalcifications formation are not fully understood. Previous studies have shown that upregulation of bone morphogenetic protein 2 (BMP-2) is associated with the occurrence of microcalcifications and tumor-associated macrophages (TAMs) in the tumor microenvironment can secrete BMP-2. The aim of this study is to elucidate the role of secretion of BMP-2 by TAMs in promoting microcalcifications of breast cancer through immunohistochemical staining and co-culturing of breast cancer cells with TAMs. Methods A total of 272 patients diagnosed with primary invasive breast cancer from January 2010 to January 2012 in the First Hospital of China Medical University were included in this study. Immunohistochemical staining of CD68 (marker of entire macrophages), CD168 (marker of the M2-like macrophages) and BMP-2 were performed on 4-μm tissue microarray (TMA) sections. Following induction, THP-1 cells were differentiated to M2-like TAMs and were then co-cultured with breast cancer cells (MCF-7). Calcifications and BMP-2 expression were analyzed by Alizarin Red S staining and western blot, respectively. Results Immunohistochemical analysis showed that the expression of CD168 was significantly increased in tissues with microcalcifications and was correlated with the expression of BMP-2 and poor prognosis. The formation of cellular microcalcifications and BMP-2 expression were significantly increased in MCF-7 cells co-cultured with TAMs compared with MCF-7 cells alone. Conclusions These findings support the hypothesis that TAMs secrete BMP-2 to induce microcalcifications in breast cancer cells and influence prognosis via multiple pathways including BMP-2 and its downstream factors.

Potential Mechanisms of miR-143/Krupple Like Factor 5 Axis in Impeding the Proliferation of Michigan Cancer Foundation-7 Breast Cancer Cell Line

2021 ◽  
Vol 11 (2) ◽  
pp. 326-332
Author(s):  
Le Ma ◽  
Zhenyu Liu ◽  
Zhimin Fan
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Breast Cancer Cells ◽  
Cell Model ◽  
Cancer Cell Line ◽  
Breast Cancer Cell Model ◽  
Underlying Mechanisms ◽  
Mcf 7

Breast cancer is one of the most prevailing cancers in females, while the cancerous heterogeneity hinders its early diagnosis and subsequent therapy. miR-143-3p is a critical mediator in malignancy development and tumorigenesis as a tumor suppressor. Its role in various tumor entities has been investigated, such as colon cancer and breast cancer. Using MCF-7 breast cancer cell model, we planned to explore the underlying mechanisms of miR-143/KLF-5 axis in retarding breast cancer cells growth. Bioinformatics analysis searched the target KLF5 of miR-143, and the miR-143-targeted mimic and inhibitor were employed to detect the changes of KLF5. After transfection of mimic miR-143, the CCK-8 reagent assessed cell proliferation. Based on optimal stimulation time, miR-143 stimulation model was established, followed by determining expression of KLF5, EGFR and PCNA via western blot and qPCR. Eventually, siRNA-KLF5 was applied to silencing KLF5 level to evaluate its role in MCF-7 cells. The transcription and translation levels of KLF5 were diminished in miR-143-mimic transfected MCF-7 cells, while enhanced in miR-143-inhibitor transfected MCF-7 cells. When MCF-7 cells were transfected with miR-143-mimic at different time points, 48 hours was found to be the optimal transfection time, with reduced transcription and translation levels of KLF5, EGFR and PCNA. The transcription and translation levels of PNCA and EGFR were declined after silencing KLF5 by siRNA. miR-143/KLF5 axis could retard the proliferation of MCF-7 breast cancer cells.

scholarly journals Mechanisms of Matrix-Induced Chemoresistance of Breast Cancer Cells—Deciphering Novel Potential Targets for a Cell Sensitization

Cancers ◽  
2018 ◽  
Vol 10 (12) ◽  
pp. 495 ◽  
Author(s):  
Bastian Jakubzig ◽  
Fabian Baltes ◽  
Svenja Henze ◽  
Martin Schlesinger ◽  
Gerd Bendas
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Signaling Pathways ◽  
Cell Lines ◽  
Intracellular Signaling ◽  
Breast Cancer Cells ◽  
Mapk Pathway ◽  
Resistance Mutations ◽  
Underlying Mechanisms ◽  
Mcf 7

Tumor cell binding to microenvironment components such as collagen type 1 (COL1) attenuates the sensitivity to cytotoxic drugs like cisplatin (CDDP) or mitoxantrone (MX), referred to as cell adhesion mediated drug resistance (CAM-DR). CAM-DR is considered as the onset for resistance mutations, but underlying mechanisms remain elusive. To evaluate CAM-DR as target for sensitization strategies, we analyzed signaling pathways in human estrogen-positive MCF-7 and triple-negative MDA-MB-231 breast cancer cells by western blot, proteome profiler array and TOP-flash assay in presence of COL1. β1-Integrins, known to bind COL1, appear as key for mediating COL1-related resistance in both cell lines that primarily follows FAK/PI3K/AKT pathway in MCF-7, and MAPK pathway in MDA-MB-231 cells. Notably, pCREB is highly elevated in both cell lines. Consequently, blocking these pathways sensitizes the cells evidently to CDDP and MX treatment. Wnt signaling is not relevant in this context. A β1-integrin knockdown of MCF-7 cells (MCF-7-β1-kd) reveals a signaling shift from FAK/PI3K/AKT to MAPK pathway, thus CREB emerges as a promising primary target for sensitization in MDA-MB-231, and secondary target in MCF-7 cells. Concluding, we provide evidence for importance of CAM-DR in breast cancer cells and identify intracellular signaling pathways as targets to sensitize cells for cytotoxicity treatment regimes.

Tumor associated macrophages antagonize antitumor effect of chemotherapy.

2017 ◽  
Vol 35 (7_suppl) ◽  
pp. 120-120
Author(s):  
Fei Chen ◽  
Shicheng Su ◽  
Erwei Song
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Antitumor Effect ◽  
Specific Treatment ◽  
Mice Model ◽  
Tumor Associated Macrophages ◽  
Treated Breast ◽  
Treated Breast Cancer ◽  
Mcf 7

120 Background: Tumor associated macrophages play an essential role in tumor progression, promoting angiogenesis, immunosupression, invasion and metastasis. However, TAMs regulation of tumor responses to chemotherapy is complicated. In different type of treatment or tumor model, TAMs can either enhance or antagonize antitumor effect of chemotherapy. Methods: We isolated TAMs from breast cancer tissues, or PBMC stimulated with culture medium of mesenchymal breast cancer cells and cocultured with breast cancer cells MCF-7 for 6-10days. After cocultured with TAMs, we treated MCF-7 with docetaxel. In vivo, we use MCF-7 with or without TAMs to generate xenografts in NOD/SCID mice and treated with docetaxel. To testify if the antagonize was dependent on specific treatment, we also treated breast cancer cells with ciaplatin. Results: With coculture of TAMs, we obversed ruduced apoptosis of docetaxel treated breast cancer cells. In mice model, TAMs co-injection xenografts antagonized the antitumor effect of docetaxel.Consisted with previous results, TAMs coculture antagonize the antitumor effect of cisplatin, suggesting the antagonize of TAMs was independent on cell cycle. Conclusions: Collectively, our study indicated the antagonize of TAMs towards chemotherapy.

scholarly journals Berberine Inhibits the Expression of SCT through miR-214-3p Stimulation in Breast Cancer Cells

2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
Congyuan Zhu ◽  
Jianping Li ◽  
Yuming Hua ◽  
Jingli Wang ◽  
Ke Wang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Mrna Expression ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Protein Levels ◽  
Transwell Invasion Assay ◽  
Underlying Mechanisms ◽  
Mcf 7

In this study, we aimed to evaluate the suppressive abilities of berberine (BBR) on MCF-7 and MDA-MB-231 cells and confirm its underlying mechanisms on miR-214-3p. We first built a panel of 18 miRNAs and 9 lncRNAs that were reported to participate in the mechanism of breast cancer. The RT-qPCR results suggested that BBR illustrated a dosage-dependent pattern in the stimulation to miR-214-3p in both MCF-7 and MDA-MB-231 cells. Then, we performed gain-and-lose function tests to validate the role of miR-214-3p contributing to the anticancer effects of BBR. Both BBR and miR-214-3p mimic reduced the cell viability, repressed migration and invasion capacities, increased rates of total apoptotic cells and ratio of Bax/Bcl-2, and increased the percentage of G2/M cells of MCF-7 and MDA-MB-231 cells by colony formation and CKK8 assay, scratch wound healing and gelatin-based 3D conformation assay, transwell invasion assay, and cell cycle analysis, respectively. However, miR-214-3p inhibitor counteracted all these effects of BBR. Based on the bioinformatics analysis and dual-luciferase reporter test, we identified binding sites between SCT and miR-214-3p. We further confirmed that BBR massively and dose-dependently reduced the mRNA expression and protein levels of SCT in both MCF-7 and MDA-231 cells. We testified that both miR-214-3p mimic and BBR could decrease the mRNA expression and protein levels of SCT, while miR-214-3p inhibitor weakened these reductions. In conclusion, BBR suppressed MCF-7 and MDA-MB-231 breast cancer cells by upregulating miR-214-3p and increasing its inhibition to SCT.

Mechanism research on the lupeol treatment on MCF-7 breast cancer cells based on cell metabonomics

2014 ◽  
Vol 32 (3) ◽  
pp. 278
Author(s):  
Dongdong SHI ◽  
Yuanyuan KUANG ◽  
Guiming WANG ◽  
Zhangxiao PENG ◽  
Yan WANG ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Mechanism Research ◽  
Mcf 7

Anticancer Potential of Calli Versus Seedling Extracts Derived from Rosmarinus officinalis and Coleus hybridus

2020 ◽  
Vol 21 (14) ◽  
pp. 1528-1538
Author(s):  
Sarah Albogami ◽  
Hadeer Darwish ◽  
Hala M. Abdelmigid ◽  
Saqer Alotaibi ◽  
Ahmed Nour El-Deen ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Transcriptional Profiling ◽  
Significant Inhibition ◽  
Rosmarinus Officinalis ◽  
Crude Extracts ◽  
Incidence And Mortality ◽  
Mcf 7

Background: In Saudi Arabia, the incidence and mortality rates of breast cancer are high. Although current treatments are effective, breast cancer cells develop resistance to these treatments. Numerous studies have demonstrated that active compounds in plant extracts, such as the phenolic compound Rosmarinic Acid (RA), exert anti-cancer effects. Objective: We investigated the anticancer properties of methanolic crude extracts of seedlings and calli of Rosmarinus officinalis and Coleus hybridus, two Lamiaceae species. Methods: MCF-7 human breast cancer cells were treated with methanolic crude extracts obtained from plant calli and seedlings generated in vitro, and cell proliferation was evaluated. Transcriptional profiling of the seedling and callus tissues was also conducted. Results: The mRNA expression levels of RA genes were higher in C. hybridus seedlings than in R. officinalis seedlings, as well as in C. hybridus calli than in R. officinalis calli, except for TAT and C4H. In addition, seedling and callus extracts of both R. officinalis and C. hybridus showed anti-proliferative effects against MCF-7 cells after 24 or 48 h of treatment. Discussion: At a low concentration of 10 μg/mL, C. hybridus calli and seedling extracts showed the most significant anti-proliferative effects after 24 and 48 h of exposure (p < 0.01); controls (doxorubicin) also showed significant inhibition, but lesser than that observed with C. hybridus (p < 0.05). Results with R. officinalis callus and seedling extracts did not significantly differ from those with untreated cells. Conclusion: Methanolic extracts of R. officinalis and C. hybridus are potentially valuable options for breast cancer treatment.

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