Biochemical differences between nano- and normal formulation of tamoxifen and other natural bioactive materials ameliorate breast cancer in experimental rats

Abstract Background Human breast cancer is the most prevalent malignancy in women all-over the world. The aim is to look further into the effectiveness of the nanoformulation of tamoxifen and even certain bioactive compounds (yeast, isoflavone, and silymarin) and their impacts on diminishing the breast cancer progression. A single medication dosage of 7,12-dimethylbenz[a]anthracene (DMBA) was administered intragastrically by fifty-four female Sprague–Dawley rats. After fourteen days of DMBA admission, the procedure protocol actually started out. At long last, all of the experimental findings assessed, tabulated, and statistically analyzed. Results In contrast to the normal groups, a substantial elevation in apoptosis and lipid peroxide was observed in all nanogroups. Conclusion The best biochemical outcome and beneficial factors which elevate the occurrence and activation of the apoptosis process have been demonstrated by nanotamoxifen.

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VN/14-1 induces ER stress and autophagy in HP-LTLC human breast cancer cells and has excellent oral pharmacokinetic profile in female Sprague Dawley rats

European Journal of Pharmacology ◽

10.1016/j.ejphar.2014.04.004 ◽

2014 ◽

Vol 734 ◽

pp. 98-104 ◽

Cited By ~ 3

Author(s):

Abhijit M. Godbole ◽

Senthilmurugan Ramalingam ◽

Vidya P. Ramamurthy ◽

Aakanksha Khandelwal ◽

Robert D. Bruno ◽

...

Keyword(s):

Breast Cancer ◽

Er Stress ◽

Cancer Cells ◽

Human Breast Cancer ◽

Breast Cancer Cells ◽

Pharmacokinetic Profile ◽

Human Breast Cancer Cells ◽

Human Breast ◽

Sprague Dawley ◽

Sprague Dawley Rats

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A New Invasion and Metastasis Molecule, Tiaml and Its Interaction With the Cytoskeleton Are Involved in Human Breast Cancer Progression

10.21236/ada392244 ◽

2000 ◽

Author(s):

Lilly Y. Bourguignon

Keyword(s):

Breast Cancer ◽

Cancer Progression ◽

Human Breast Cancer ◽

Breast Cancer Progression ◽

Human Breast ◽

Invasion And Metastasis

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Down-Regulation of the Proteoglycan Decorin Fills in the Tumor-Promoting Phenotype of Ionizing Radiation-Induced Senescent Human Breast Stromal Fibroblasts

Cancers ◽

10.3390/cancers13081987 ◽

2021 ◽

Vol 13 (8) ◽

pp. 1987

Author(s):

Eleni Mavrogonatou ◽

Adamantia Papadopoulou ◽

Asimina Fotopoulou ◽

Stathis Tsimelis ◽

Heba Bassiony ◽

...

Keyword(s):

Breast Cancer ◽

Ionizing Radiation ◽

Cancer Progression ◽

Breast Cancer Cell Lines ◽

Phenotypic Trait ◽

Mrna Levels ◽

Human Breast ◽

Down Regulation ◽

Stromal Fibroblasts ◽

Poor Prognostic Factor

Down-regulation of the small leucine-rich proteoglycan decorin in the stroma is considered a poor prognostic factor for breast cancer progression. Ionizing radiation, an established treatment for breast cancer, provokes the premature senescence of the adjacent to the tumor stromal fibroblasts. Here, we showed that senescent human breast stromal fibroblasts are characterized by the down-regulation of decorin at the mRNA and protein level, as well as by its decreased deposition in the pericellular extracellular matrix in vitro. Senescence-associated decorin down-regulation is a long-lasting process rather than an immediate response to γ-irradiation. Growth factors were demonstrated to participate in an autocrine manner in decorin down-regulation, with bFGF and VEGF being the critical mediators of the phenomenon. Autophagy inhibition by chloroquine reduced decorin mRNA levels, while autophagy activation using the mTOR inhibitor rapamycin enhanced decorin transcription. Interestingly, the secretome from a series of both untreated and irradiated human breast cancer cell lines with different molecular profiles inhibited decorin expression in young and senescent stromal fibroblasts, which was annulled by SU5402, a bFGF and VEGF inhibitor. The novel phenotypic trait of senescent human breast stromal fibroblasts revealed here is added to their already described cancer-promoting role via the formation of a tumor-permissive environment.

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Stromal CCL5 Promotes Breast Cancer Progression by Interacting with CCR3 in Tumor Cells

International Journal of Molecular Sciences ◽

10.3390/ijms22041918 ◽

2021 ◽

Vol 22 (4) ◽

pp. 1918

Author(s):

Mio Yamaguchi ◽

Kiyoshi Takagi ◽

Koki Narita ◽

Yasuhiro Miki ◽

Yoshiaki Onodera ◽

...

Keyword(s):

Breast Cancer ◽

Breast Carcinoma ◽

Tumor Progression ◽

Tumor Cells ◽

Cancer Progression ◽

Stromal Cells ◽

Human Breast Carcinoma ◽

Breast Cancer Patients ◽

Breast Carcinomas ◽

Human Breast

Chemokines secreted from stromal cells have important roles for interactions with carcinoma cells and regulating tumor progression. C-C motif chemokine ligand (CCL) 5 is expressed in various types of stromal cells and associated with tumor progression, interacting with C-C chemokine receptor (CCR) 1, 3 and 5 expressed in tumor cells. However, the expression on CCL5 and its receptors have so far not been well-examined in human breast carcinoma tissues. We therefore immunolocalized CCL5, as well as CCR1, 3 and 5, in 111 human breast carcinoma tissues and correlated them with clinicopathological characteristics. Stromal CCL5 immunoreactivity was significantly correlated with the aggressive phenotype of breast carcinomas. Importantly, this tendency was observed especially in the CCR3-positive group. Furthermore, the risk of recurrence was significantly higher in the patients with breast carcinomas positive for CCL5 and CCR3 but negative for CCR1 and CCR5, as compared with other patients. In summary, the CCL5-CCR3 axis might contribute to a worse prognosis in breast cancer patients, and these findings will contribute to a better understanding of the significance of the CCL5/CCRs axis in breast carcinoma microenvironment.

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Exploration of anti-breast cancer effects of Terminalia chebula extract on DMBA-induced mammary carcinoma in Sprague Dawley rats

Future Journal of Pharmaceutical Sciences ◽

10.1186/s43094-020-00124-z ◽

2020 ◽

Vol 6 (1) ◽

Author(s):

Deena Priscilla Henry ◽

Jasmine Ranjan ◽

Rajesh Kumar Murugan ◽

Annapoorani Sivanantham ◽

Manikandan Alagumuthu

Keyword(s):

Breast Cancer ◽

Plant Extract ◽

Mammary Carcinoma ◽

Future Perspective ◽

Terminalia Chebula ◽

Sprague Dawley ◽

Analytical Technique ◽

Isolation And Characterization ◽

Sprague Dawley Rats ◽

Mcf 7

Abstract Background Plant extracts are effectively acting as the natural medicinal cocktail, non-side effective, efficacious, and freely available. The present study aimed to unveil the pharmacological and medicinal effects of Terminalia chebula plant extract in 7,12-dimethylbenzanthracene (DMBA)-induced mammary carcinoma in Sprague Dawley rats. The plant extract obtained was subjected to in vivo antioxidant and anticancer studies in various concentrations after an analytical technique such as FTIR, GCMS, and HPLC-based chemo-profiling in Sprague Dawley rats. Results Apart from the antiproliferative effect on breast cancer cell line (MCF-7) and normal breast epithelial cells (MCF-10a), we have measured the changes in body weight, along with other tumor parameters such as tumor volume, tumor incidence, tumor weight, tumor burden, serum biochemical parameters, and histopathological findings of breast tissue. As the oxidative stress further enhances the development of cancer, the antioxidant property of the plant extract demonstrates its use against cancer treatment. One hundred fifty milligrams per milliliter (IC50 250 μg/mL) concentration of the ethanolic extract was vital for the proliferation of MCF-7 cell lines (Fig. 7a). Meanwhile, 300 μg/mL (IC50 150 μg/mL) was an effective dose to attain a maximum HDAC inhibition of 78%. Also, the normal liver and kidney functioning revealed the non-toxicity nature of the plant. Conclusion Terminalia chebula could be one of the effective naturally obtained anti-breast cancer medications. Isolation and characterization of individual bioactive compounds of T. chebula would be the future perspective.

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Proteomic Portrait of Human Breast Cancer Progression Identifies Novel Prognostic Markers

Cancer Research ◽

10.1158/0008-5472.can-11-3711 ◽

2012 ◽

Vol 72 (9) ◽

pp. 2428-2439 ◽

Cited By ~ 88

Author(s):

Tamar Geiger ◽

Stephen F. Madden ◽

William M. Gallagher ◽

Juergen Cox ◽

Matthias Mann

Keyword(s):

Breast Cancer ◽

Cancer Progression ◽

Human Breast Cancer ◽

Prognostic Markers ◽

Breast Cancer Progression ◽

Human Breast

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Steroid receptors in human breast tumorigenesis and breast cancer progression

Biomedicine & Pharmacotherapy ◽

10.1016/s0753-3322(01)00157-3 ◽

2002 ◽

Vol 56 (2) ◽

pp. 65-77 ◽

Cited By ~ 38

Author(s):

L.C Murphy ◽

P Watson

Keyword(s):

Breast Cancer ◽

Cancer Progression ◽

Steroid Receptors ◽

Breast Cancer Progression ◽

Human Breast ◽

Breast Tumorigenesis

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Visfatin Mediates Malignant Behaviors through Adipose-Derived Stem Cells Intermediary in Breast Cancer

Cancers ◽

10.3390/cancers12010029 ◽

2019 ◽

Vol 12 (1) ◽

pp. 29 ◽

Cited By ~ 3

Author(s):

Jyun-Yuan Huang ◽

Yen-Yun Wang ◽

Steven Lo ◽

Ling-Ming Tseng ◽

Dar-Ren Chen ◽

...

Keyword(s):

Breast Cancer ◽

Stem Cells ◽

Cancer Progression ◽

Human Breast Cancer ◽

Breast Cancer Progression ◽

Akt Pathway ◽

Adipose Derived Stem Cells ◽

Human Breast ◽

Akt Inhibitor ◽

Promoting Effect

Adipose-derived stem cells (ADSCs) have been implicated in tumor growth and metastasis in breast cancer. ADSCs exhibit tumor tropism, and are of increasing clinical relevance due to the autologous fat grafting for breast reconstruction. Although we have previously shown that a high level of the adipocytokine visfatin in human breast cancer tissues correlated with tumor progression mediated by cAbl and STAT3, the effects of visfatin in the tumor microenvironment are unclear. To understand how visfatin modulates breast cancer within the tumor-stromal environment, we examined determinants of breast cancer progression using a visfatin-primed ADSCs-tumor co-culture model. ADSCs were isolated from tumor-free adipose tissue adjacent to breast tumors. ADSCs were treated with or without visfatin for 48 h and then collected for co-culture with breast cancer cell line MDA-MB-231 for 72 h in a transwell system. We found that the MDA-MB-231 cells co-cultured with visfatin-treated ADSCs (vADSCs) had higher levels of cell viability, anchorage independent growth, migration, invasion, and tumorsphere formation than that co-cultured with untreated ADSCs (uADSCs). Growth differentiation factor 15 (GDF15) upregulation was found in the co-culture conditioned medium, with GDF15 neutralizing antibody blocking the promoting effect on MDA-MB-231 in co-culture. In addition, a GDF15-induced AKT pathway was found in MDA-MB-231 and treatment with PI3K/AKT inhibitor also reversed the promoting effect. In an orthotopic xenograft mouse model, MDA-MB-231 co-injected with vADSCs formed a larger tumor mass than with uADSCs. Positive correlations were noted between visfatin, GDF15, and phosphor-AKT expressions in human breast cancer specimens. In conclusion, visfatin activated GDF15-AKT pathway mediated via ADSCs to facilitate breast cancer progression.

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