MicroRNA-7 agomir is a potential bioactive material for breast cancer therapy by inhibiting breast cancer stem cell tumorigenicity

2021 ◽  
Vol 11 (6) ◽  
pp. 824-831
Author(s):  
Miao Li ◽  
Jun Dou ◽  
Meng Pan ◽  
Hui Xu ◽  
Zhiye Xu
Keyword(s):  
Breast Cancer ◽  
Tumor Growth ◽  
Human Breast Cancer ◽  
Human Breast Cancer Cell ◽  
Breast Cancer Cell Lines ◽  
Human Breast ◽  
Cd44 Expression ◽  
Bioactive Material ◽  
Tumor Tissues ◽  
Mcf 7

Breast cancer stem cells (BCSCs) have been proven to be the root of development, metastasis and recurrence of breast cancer. It is crucial to explore the underlying paths of regulating BCSCs for breast cancer treatment. Many bioactive materials have been developed to modify therapeutic drugs or as drug delivery vehicles for tumor treatment. In this study, we aimed to probe the effect of microRNA-7 (miR-7) agomir, a potential bioactive material, in breast cancer treatment by reducing tumorigenicity of BCSCs. Magnetic activated cell sorting was used to isolate the BCSCs from the MDA-MB-231 and LD cells. Protein array was performed to screen differentially expressed proteins. The expression levels for miR-7 and CD44 in human breast cancer cell lines were detected by Quantitative real-time PCR (q-PCR), Western blot (WB) and Flow cytometry (FCM) assays. Lentiviral recombinants were constructed to infect the primary human breast cancer cells to obtain the cells stably overexpressing miR-7. BCSCs xenograft model was established in NOD/SCID mice and the tumor tissues were analyzed by hematoxylin-eosin staining (HE) and immunohistochemistry (IHC). We found that miR-7 agomir can inhibit the tumor growth in mice and the expression of CD44 in the tumor tissues treated with miR-7 agomir was 2.4 times lower than that of control treatment from the protein array results. Among the MDA-MB- 231, MCF-7, SK-BR-3 and LD human breast cancer cell lines, the expression of CD44 was downregulated in the MCF-7 cells with relatively high miR-7 expression. Overexpression of miR-7 effectively reduced the CD44 expression in LD cells. Furthermore, compared with control and chemotherapy treatments, the mouse tumor growth was significantly inhibited in the mice infected with Lenti-miR-7-BCSCs, concomitantly decreasing the CD44 expression in tumor tissues. These findings suggest that miR-7 agomir can be used as a potential bioactive material to inhibit tumor growth in BCSCs xenograft mouse model by downregulating the CD44 expression and reducing BCSCs tumorigenicity.

scholarly journals New Isoflavanes from Spatholobus suberectus and Their Cytotoxicity against Human Breast Cancer Cell Lines

Molecules ◽  
2019 ◽  
Vol 24 (18) ◽  
pp. 3218 ◽  
Author(s):  
Fu Peng ◽  
Huan Zhu ◽  
Chun-Wang Meng ◽  
Yan-Rui Ren ◽  
Ou Dai ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Human Breast Cancer ◽  
Human Breast Cancer Cell ◽  
Breast Cancer Cell Lines ◽  
Human Breast ◽  
Spatholobus Suberectus ◽  
Mcf 7

The rattans of Spatholobus suberectus Dunn are a traditional Chinese medicine activating blood circulation and removing stasis. They have often been used for the traditional Chinese medicinal treatment of breast cancer in modern China. In this study, four novel isoflavanes (1–3 and 5) and four known analogues (4 and 6–8) were isolated from an ethanolic extract of the rattans of S. suberectus. Their structures were elucidated by extensive spectroscopic analyses and electronic circular dichroism studies. MCF-7 and MDA-MB-231 human breast cancer cell lines were used to evaluate the cytotoxic effects of the isolates. Interestingly, compounds 1 and 2 only inhibited the proliferation of MCF-7 cells, while compound 6 showed a selective cytotoxicity against MDA-MB-231 cells. However, compound 4 had significant cytotoxicity against both MCF-7 and MDA-MB-231 cell lines.

Peroxisome proliferator-activated receptor ? in the human breast cancer cell lines MCF-7 and MDA-MB-231

2002 ◽  
Vol 34 (4) ◽  
pp. 165-171 ◽  
Author(s):  
Kate M. Suchanek ◽  
Fiona J. May ◽  
Jodie A. Robinson ◽  
Won Jae Lee ◽  
Nicola A. Holman ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Lines ◽  
Breast Cancer Cell ◽  
Human Breast Cancer ◽  
Human Breast Cancer Cell ◽  
Breast Cancer Cell Lines ◽  
Peroxisome Proliferator ◽  
Human Breast ◽  
Peroxisome Proliferator Activated Receptor ◽  
Mcf 7

scholarly journals Calcitonin binding and degradation by two cultured human breast cancer cell lines (MCF 7 and T 47D)

1981 ◽  
Vol 196 (2) ◽  
pp. 513-520 ◽  
Author(s):  
D M Findlay ◽  
V P Michelangeli ◽  
J M Moseley ◽  
T J Martin
Keyword(s):  
Breast Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Salmon Calcitonin ◽  
Human Breast Cancer ◽  
Human Breast Cancer Cell ◽  
Breast Cancer Cell Lines ◽  
Human Breast ◽  
Mcf 7

Two human breast cancer cell lines (MCF 7 and T 47D) possess calcitonin-responsive adenylate cyclase systems. Suspended cells of both lines specifically bound 125I-labelled salmon calcitonin with mean dissociation constants of 1.7 nM (MCF 7) and 1.4 nM (T 47D); mean receptor numbers were 5300 and 24400 per cell respectively. Measurement of specific binding to MCF 7 cells was obscured by rapid and substantial degradation of the labelled hormone. Degradation of 125I-labelled salmon calcitonin: (i) was of high capacity; (ii) lacked the specificity displayed by 125I-labelled salmon calcitonin binding to the same cells; and (iii) was not related to binding since cell incubation supernatants retained full degrading activity. The degrading activity was inhibited by corticotropin (1-24)-tetracosapeptide, insulin and bacitracin. Inclusion of bacitracin in the incubation resulted in apparently fewer numbers of lower affinity receptors on MCF 7 cells, whereas these parameters were identical to T 47D cells incubated in the presence or absence of bacitracin. Eel [2-aminosuberic acid 1,7]-calcitonin was resistant to proteolysis in the presence of either cell line. Analysis of hormone-receptor interactions with calcitonin-responsive cells should take account of potent calcitonin-degrading activities in some cell lines.

scholarly journals Cellular and molecular crosstalk between leptin receptor and estrogen receptor-α in breast cancer: molecular basis for a novel therapeutic setting

2010 ◽  
Vol 17 (2) ◽  
pp. 373-382 ◽  
Author(s):  
Roberta Fusco ◽  
Mario Galgani ◽  
Claudio Procaccini ◽  
Renato Franco ◽  
Giuseppe Pirozzi ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Lines ◽  
Human Breast Cancer ◽  
Leptin Receptor ◽  
Estrogen Receptor Α ◽  
Human Breast Cancer Cell ◽  
Breast Cancer Cell Lines ◽  
Human Breast ◽  
Increased Risk ◽  
Mcf 7

Obesity is associated with an increased risk of breast cancer. A number of adipocytokines are increased in obesity causing low-level chronic inflammation associated with an increased risk of tumors. The adipocytokine leptin shows profound anti-obesity and pro-inflammatory activities. We have hypothesized that in common obesity, high circulating leptin levels might contribute to an increased risk of breast cancer by affecting mammary cell proliferation and survival. Leptin exerts its activity not only through leptin receptor (LepR), but also through crosstalk with other signaling systems implicated in tumorigenesis. In this study, we focused our attention on the relationship between the leptin/LepR axis and the estrogen receptor-α (ERα). To this aim, we utilized two human breast cancer cell lines, one ERα-positive cell line (MCF 7) and the other ERα-negative cell line (MDA-MB 231). We observed that the two cell lines had a different sensitivity to recombinant leptin (rleptin): on MCF 7 cells, rleptin induced a strong phosphorylation of the signal transducer and activator of transcription (STAT) 3 and of the extracellular related kinase 1/2 pathways with an increased cell viability and proliferation associated with an increased expression of ERα receptor. This response was not present in the MDA-MB 231 cells. The effects induced by leptin were lost when LepR was neutralized using either a monoclonal inhibitory antibody to LepR or LepR gene-silencing siRNA. These data suggest that there is a bidirectional communication between LepR and ERα, and that neutralization and/or inactivation of LepR inhibits proliferation and viability of human breast cancer cell lines. This evidence was confirmed by ex vivo studies, in which we analyzed 33 patients with breast cancer at different stages of disease, and observed that there was a statistically significant correlation between the expression of LepR and ERα. In conclusion, this study suggests a crosstalk between LepR and ERα, and could envisage novel therapeutic settings aimed at targeting the LepR in breast cancers.

Sign in / Sign up

Export Citation Format

Share Document