Ceramide targets xIAP and cIAP1 to sensitize metastatic colon and breast cancer cells to apoptosis induction to suppress tumor progression

As chemotherapeutic backbone for breast cancer therapy, doxorubicin showed various side effects and induced resistancy of breast cancer cells. Development of targeted therapy on breast cancer focused on combinatorial therapy of doxorubicin and molecular targeted agents. PGV-0 and PGV-1, a curcumin analogue showed potency as co-chemotherapeutic agent with doxorubicin. Our previous study of PGV-0 and PGV-1 showed cytotoxic activity in T47D cells. Therefore, the aim of this research is to examine the synergistic effect of PGV-0, PGV-1 on the cytotoxic activity of doxorubicin through cell cycle modulation and apoptotic induction on MCF-7 breast cancer cell lines. The cytotoxic assay of PGV-0, PGV-1, doxorubicin, and their combination were carried out by using MTT assay. Cell cycle distribution and apoptosis were determined by flowcytometer FACS-Calibur and the flowcytometry data was analyzed using Cell Quest program. Single treatment of PGV-0, PGV-1 and doxorubicin showed cytotoxic effect on MCF-7 with cell viability IC50 value 50 µM, 6 µM and 350 nM respectively. Single treatment of Doxorubicin 175 nM induced G2/M arrest. Single treatment of PGV-0 5 µM induced G2/M arrest while in higher dose 12.5 µM, PGV-0 induced apoptosis. Combination of doxorubicin 175 nM and PGV-0 5 µM induced apoptosis. Combination of doxorubicin 175 nM and PGV-0 12.5 µM also increased apoptosis induction. Single treatment of PGV-1 0.6 µM induced G1 arrest while in higher dose 1.5 µM, PGV-1 induced apoptosis. Combination of doxorubicin 175 nM and PGV-1 0.6 µM induced apoptosis. Combination of doxorubicin 175 nM and PGV-0 1.5 µM also increased apoptosis induction. PGV-0 and PGV-1 are potential to be delevoped as co-chemotherapeutic agent for breast cancer by inducing apoptosis and cell cycle modulation, but the molecular mechanism need to be explored detail. Key words: PGV-0, PGV-1, doxorubicin, co-chemotherapy, breast cancer, cell cycle arrest, apoptosis

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Exosomal miR-222 from adriamycin-resistant MCF-7 breast cancer cells promote macrophages M2 polarization via PTEN/Akt to induce tumor progression

Aging ◽

10.18632/aging.202802 ◽

2021 ◽

Author(s):

Wei-Xian Chen ◽

Dan-Dan Wang ◽

Bei Zhu ◽

Yi-Zhi Zhu ◽

Lin Zheng ◽

...

Keyword(s):

Breast Cancer ◽

Tumor Progression ◽

Cancer Cells ◽

Breast Cancer Cells ◽

M2 Polarization ◽

Mcf 7

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Characteristics of apoptosis induction in human breast cancer cells treated with a ceramidase inhibitor

Cytotechnology ◽

10.1007/s10616-020-00436-1 ◽

2020 ◽

Vol 72 (6) ◽

pp. 907-919

Author(s):

Hüseyin İzgördü ◽

Canan Vejselova Sezer ◽

Emre Çömlekçi ◽

Hatice Mehtap Kutlu

Keyword(s):

Breast Cancer ◽

Cancer Cells ◽

Human Breast Cancer ◽

Breast Cancer Cells ◽

Apoptosis Induction ◽

Human Breast Cancer Cells ◽

Human Breast

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MSCs inhibit tumor progression and enhance radiosensitivity of breast cancer cells by down-regulating Stat3 signaling pathway

Cell Death and Disease ◽

10.1038/s41419-018-0949-3 ◽

2018 ◽

Vol 9 (10) ◽

Cited By ~ 20

Author(s):

Ningning He ◽

Yangyang Kong ◽

Xudan Lei ◽

Yang Liu ◽

Jinhan Wang ◽

...

Keyword(s):

Breast Cancer ◽

Tumor Progression ◽

Cancer Cells ◽

Signaling Pathway ◽

Breast Cancer Cells ◽

Stat3 Signaling ◽

Stat3 Signaling Pathway

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Periodontal inflammation recruits distant metastatic breast cancer cells by increasing myeloid-derived suppressor cells

Oncogene ◽

10.1038/s41388-019-1084-z ◽

2019 ◽

Vol 39 (7) ◽

pp. 1543-1556 ◽

Cited By ~ 5

Author(s):

Ran Cheng ◽

Sandrine Billet ◽

Chuanxia Liu ◽

Subhash Haldar ◽

Diptiman Choudhury ◽

...

Keyword(s):

Breast Cancer ◽

Tumor Progression ◽

Cancer Cells ◽

Cancer Progression ◽

Breast Cancer Cells ◽

Periodontal Diseases ◽

Metastatic Breast ◽

Metastatic Progression ◽

Premetastatic Niche ◽

Periodontal Inflammation

Abstract Periodontal diseases can lead to chronic inflammation affecting the integrity of the tooth supporting tissues. Recently, a striking association has been made between periodontal diseases and primary cancers in the absence of a mechanistic understanding. Here we address the effect of periodontal inflammation (PI) on tumor progression, metastasis, and possible underlining mechanisms. We show that an experimental model of PI in mice can promote lymph node (LN) micrometastasis, as well as head and neck metastasis of 4T1 breast cancer cells, both in early and late stages of cancer progression. The cervical LNs had a greater tumor burden and infiltration of MDSC and M2 macrophages compared with LNs at other sites. Pyroptosis and the resultant IL-1β production were detected in patients with PI, mirrored in mouse models. Anakinra, IL-1 receptor antagonist, limited metastasis, and MDSC recruitment at early stages of tumor progression, but failed to reverse established metastatic tumors. PI and the resulting production of IL-1β was found to promote CCL5, CXCL12, CCL2, and CXCL5 expression. These chemokines recruit MDSC and macrophages, finally enabling the generation of a premetastatic niche in the inflammatory site. These findings support the idea that periodontal inflammation promotes metastasis of breast cancer by recruiting MDSC in part by pyroptosis-induced IL-1β generation and downstream CCL2, CCL5, and CXCL5 signaling in the early steps of metastasis. These studies define the role for IL-1β in the metastatic progression of breast cancer and highlight the need to control PI, a pervasive inflammatory condition in older patients.

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Epinephrine Infiltration of Adipose Tissue Impacts MCF7 Breast Cancer Cells and Total Lipid Content

International Journal of Molecular Sciences ◽

10.3390/ijms20225626 ◽

2019 ◽

Vol 20 (22) ◽

pp. 5626 ◽

Cited By ~ 3

Author(s):

Pierre Avril ◽

Luciano Vidal ◽

Sophie Barille-Nion ◽

Louis-Romée Le Nail ◽

Françoise Redini ◽

...

Keyword(s):

Breast Cancer ◽

Adipose Tissue ◽

Tumor Progression ◽

Cancer Cells ◽

Conditioned Medium ◽

Lipid Composition ◽

Breast Cancer Cells ◽

Quiescent State ◽

Mcf7 Cells ◽

Mesenchymal Transition

Background: Considering the positive or negative potential effects of adipocytes, depending on their lipid composition, on breast tumor progression, it is important to evaluate whether adipose tissue (AT) harvesting procedures, including epinephrine infiltration, may influence breast cancer progression. Methods: Culture medium conditioned with epinephrine-infiltrated adipose tissue was tested on human Michigan Cancer Foundation-7 (MCF7) breast cancer cells, cultured in monolayer or in oncospheres. Lipid composition was evaluated depending on epinephrine-infiltration for five patients. Epinephrine-infiltrated adipose tissue (EI-AT) or corresponding conditioned medium (EI-CM) were injected into orthotopic breast carcinoma induced in athymic mouse. Results: EI-CM significantly increased the proliferation rate of MCF7 cells Moreover EI-CM induced an output of the quiescent state of MCF7 cells, but it could be either an activator or inhibitor of the epithelial mesenchymal transition as indicated by gene expression changes. EI-CM presented a significantly higher lipid total weight compared with the conditioned medium obtained from non-infiltrated-AT of paired-patients. In vivo, neither the EI-CM or EI-AT injection significantly promoted MCF7-induced tumor growth. Conclusions: Even though conditioned media are widely used to mimic the secretome of cells or tissues, they may produce different effects on tumor progression, which may explain some of the discrepancy observed between in vitro, preclinical and clinical data using AT samples.

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COMBINATION OF HEDYOTIS CORYMBOSA L. AND TINOSPORA CRISPA ETHANOLIC EXTRACT INCREASE CISPLATIN CYTOTOXICITY ON T47D BREAST CANCER CELLS

Asian Journal of Pharmaceutical and Clinical Research ◽

10.22159/ajpcr.2018.v11i7.25607 ◽

2018 ◽

Vol 11 (7) ◽

pp. 171 ◽

Cited By ~ 1

Author(s):

Rollando Rollando

Keyword(s):

Breast Cancer ◽

Cell Cycle ◽

Cancer Cells ◽

Breast Cancer Cells ◽

Cytotoxic Effect ◽

Ethanolic Extract ◽

T47d Cell ◽

Apoptosis Induction ◽

Cell Accumulation ◽

Cell Cycle Modulation

Objective: Ursolic acid was a compound found in Hedyotis corymbosa L., (HCoL) while berberine found in Tinospora crispa (TCa) which are proven to have cytotoxic effect to cancer cells. This research aims to review the effect of cisplatin, ethanolic extract of HCoL and TCa to the sensitivity increase on breast cancer cells, which will be confirmed through apoptosis induction and cell cycle modulation.Methods: The cytotoxic effect was tested using 3-(4,5-dimethylthiazol-2-il)-2,5-diphenyltetrazolium bromide assay on T47D cell using the IC50 parameter. The combination was tested by determining their combination index (CI) and cell viability. The combination effect of apoptosis induction and cell cycle modulation was observed using flow cytometry method.Results: The cytotoxic test result of the combination shows CI value of below 1 at the concentration of HCoL ethanolic extract as much as 1 μg/mL, TCa ethanolic extract as much as 6 μg/mL, and cisplatin as much as 2,5 μM. The combination of HCoL ethanolic extract, TCa ethanolic extract, and cisplatin results in phase S cell accumulation (29.98%) on breast cancer cell T47D and was able to induce apoptosis.Conclusion: The result proves that ethanolic extract of HCoL and TCa can be developed as a cochemotherapeutic agent with cisplatin to increase the effectivity of breast cancer treatment.

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