scholarly journals Anti-cancer therapeutic benefit of red guava extracts as a potential therapy in combination with doxorubicin or targeted therapy for triple-negative breast cancer cells

2020 ◽  
Vol 17 (8) ◽  
pp. 1015-1022 ◽  
Author(s):  
Hsiao-Chun Liu ◽  
Chien-Chuan Chiang ◽  
Ching-Hsiang Lin ◽  
Chien-Sheng Chen ◽  
Chyou-Wei Wei ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Targeted Therapy ◽  
Cancer Cells ◽  
Triple Negative Breast Cancer ◽  
Breast Cancer Cells ◽  
Triple Negative ◽  
Therapeutic Benefit ◽  
Anti Cancer

scholarly journals Anti-Cancer Effects of Sulfasalazine and Vitamin E Succinate in MDA-MB 231 Triple-Negative Breast Cancer Cells

2019 ◽  
Vol 16 (4) ◽  
pp. 494-500 ◽  
Author(s):  
Chyou-Wei Wei ◽  
Yung-Luen Yu ◽  
Ji-Ying Lu ◽  
Yu-Ting Hung ◽  
Hsiao-Chun Liu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Vitamin E ◽  
Cancer Cells ◽  
Triple Negative Breast Cancer ◽  
Breast Cancer Cells ◽  
Triple Negative ◽  
Vitamin E Succinate ◽  
Anti Cancer

Anti-cell growth and anti-cancer stem cell activities of the non-canonical hedgehog inhibitor GANT61 in triple-negative breast cancer cells

Breast Cancer ◽  
2017 ◽  
Vol 24 (5) ◽  
pp. 683-693 ◽  
Author(s):  
Yoshikazu Koike ◽  
Yusuke Ohta ◽  
Wataru Saitoh ◽  
Tetsumasa Yamashita ◽  
Naoki Kanomata ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Stem Cell ◽  
Cell Growth ◽  
Cancer Stem Cell ◽  
Cancer Cells ◽  
Triple Negative Breast Cancer ◽  
Breast Cancer Cells ◽  
Triple Negative ◽  
Anti Cancer ◽  
Hedgehog Inhibitor

scholarly journals Molecular mechanism of anti-cancer activity of phycocyanin in triple-negative breast cancer cells

BMC Cancer ◽  
2015 ◽  
Vol 15 (1) ◽  
Author(s):  
Mathangi Ravi ◽  
Shilpa Tentu ◽  
Ganga Baskar ◽  
Surabhi Rohan Prasad ◽  
Swetha Raghavan ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Molecular Mechanism ◽  
Triple Negative Breast Cancer ◽  
Breast Cancer Cells ◽  
Triple Negative ◽  
Anti Cancer ◽  
Cancer Activity

scholarly journals Novel Melatonin, Estrogen, and Progesterone Hormone Therapy Demonstrates Anti-Cancer Actions in MCF-7 and MDA-MB-231 Breast Cancer Cells

2020 ◽  
Vol 14 ◽  
pp. 117822342092463
Author(s):  
Mahmud Hasan ◽  
Erin Browne ◽  
Laura Guarinoni ◽  
Travis Darveau ◽  
Katherine Hilton ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Hormone Therapy ◽  
Cancer Cells ◽  
Triple Negative Breast Cancer ◽  
Breast Cancer Cells ◽  
Triple Negative ◽  
Anti Cancer ◽  
And Migration ◽  
Mcf 7 ◽  
Proliferation And Migration

A novel melatonin, estrogen, and progesterone hormone therapy was developed as a safe bio-identical alternative hormone therapy for menopausal women based on the Women’s Health Initiative findings that PremPro™ increased breast cancer risk and mortality of all types of breast cancer in postmenopausal women. For HER2 breast cancer, melatonin, estrogen, and progesterone delayed tumor onset and reduced tumor incidence in neu female mice. For other breast cancers, its actions are unknown. In this study, melatonin, estrogen, and progesterone hormone therapy were assessed in human ER+ (MCF-7) and triple negative breast cancer (MDA-MB-231) cells, and found to decrease proliferation and migration of both breast cancer lines. Inhibition of MEK1/2 and 5 using PD98059 and BIX02189, respectively, inhibited proliferation and migration in MDA-MB-231 cells and proliferation in MCF-7 cells; however, when combined with melatonin, estrogen, and progesterone, BIX02189 blocked melatonin, estrogen, and progesterone–mediated inhibition of migration in MCF-7 cells and induced Elf-5. For MDA-MB-231 cells, BIX02189 combined with melatonin, estrogen, and progesterone inhibited proliferation and increased pERK1/2 and β1-INTEGRIN; levels of pERK5 remained low/nearly absent in both breast cancer lines. These findings demonstrate novel anti-cancer actions of melatonin, estrogen, and progesterone in ER+ and triple negative breast cancer cells through intricate MEK1/2- and MEK5-associated signaling cascades that favor anti-proliferation and anti-migration.

Supramolecular magnetonanohybrids for multimodal targeted therapy of triple-negative breast cancer cells

2020 ◽  
Vol 8 (32) ◽  
pp. 7166-7188 ◽  
Author(s):  
Alexandra A. P. Mansur ◽  
Herman S. Mansur ◽  
Alice G. Leonel ◽  
Isadora C. Carvalho ◽  
Manuela C. G. Lage ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Targeted Therapy ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Triple Negative Breast Cancer ◽  
Breast Cancer Cells ◽  
Triple Negative

All-in-one nanosoldier on a targeted mission: killing the triple-negative breast cancer cell enemy.

scholarly journals High Glucose Represses the Anti-Proliferative and Pro-Apoptotic Effect of Metformin in Triple Negative Breast Cancer Cells

Biomolecules ◽  
2019 ◽  
Vol 9 (1) ◽  
pp. 16 ◽  
Author(s):  
Sharon Varghese ◽  
Samson Mathews Samuel ◽  
Elizabeth Varghese ◽  
Peter Kubatka ◽  
Dietrich Büsselberg
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Triple Negative Breast Cancer ◽  
High Glucose ◽  
Breast Cancer Cells ◽  
Triple Negative ◽  
Mtor Pathway ◽  
P Value ◽  
Anti Cancer

Metformin, the most widely prescribed anti-diabetic drug, is shown to possess anti-cancer potential in treatment of cancers, including breast cancer; decreases breast cancer risk; and improves overall survival. However, reports suggest that higher glucose concentrations may negatively impact the anti-cancer efficacy of metformin. Therefore, we examined the anti-cancer potential of metformin in triple-negative breast cancer cells (TNBCs) exposed to different glucose (25 mM, 5.5 mM and zero glucose/glucose-starved) conditions. Our data indicates that a high glucose (25 mM) concentration (mimicking diabetes) significantly abrogated the effect of metformin on cell proliferation, cell death and cell cycle arrest in addition to loss of efficacy in inhibition of the mTOR pathway, a key metabolic pathway in TNBC cells. The mTOR pathway is activated in TNBCs compared to other subtypes of breast cancer, regulates the synthesis of proteins that are critical for the growth and survival of cancer cells and its activation is correlated to poor outcomes among TNBC patients, while also contributing to metastatic progression and development of resistance to chemotherapy/radiotherapy. Our studies were performed in two different types of TNBCs, MDA-MB-231 cells (mesenchymal stem cell-like (MSL)) and MDA-MB-468 (basal like-1 (BL-1)). Interestingly, lower concentrations of metformin (50, 100, 250, and 500 μM) significantly increased cell proliferation in 25 mM glucose exposed MDA-MB-231 cells, an effect which was not observed in MDA-MB-468 cells, indicating that the effective concentration of metformin when used as anti-cancer drug in TNBCs may have to be determined based on cell type and blood glucose concentration. Our data indicates that metformin treatment was most effective under zero glucose/glucose-starved conditions in MDA-MB-468 with a significant increase in the apoptotic population (62.3 ± 1.5%; p-value < 0.01). Under 5.5 mM glucose conditions in both MDA-MB-231 and MDA-MB-468 cells our data showed reduced viability of 73.56 ± 2.53%; p-value < 0.05 and 70.49 ± 1.68%; p-value < 0.001, respectively, along with a significant increase in apoptotic populations of both cell types. Furthermore, metformin (2 mM) inhibited the mTOR pathway and its downstream components under zero glucose/glucose-starved conditions indicating that using metformin in combination with agents that inhibit the glycolytic pathway should be more beneficial for the treatment of triple-negative breast cancers in diabetic individuals.

scholarly journals Application of a Biphasic Mathematical Model of Cancer Cell Drug Response for Formulating Potent and Synergistic Targeted Drug Combinations to Triple Negative Breast Cancer Cells

Cancers ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1087
Author(s):  
Jinyan Shen ◽  
Li Li ◽  
Niall G. Howlett ◽  
Paul S. Cohen ◽  
Gongqin Sun
Keyword(s):  
Breast Cancer ◽  
Mathematical Model ◽  
Targeted Therapy ◽  
Cancer Cells ◽  
Cell Lines ◽  
Triple Negative Breast Cancer ◽  
Breast Cancer Cells ◽  
Triple Negative ◽  
Drug Combinations ◽  
Targeted Drug

Triple negative breast cancer is a collection of heterogeneous breast cancers that are immunohistochemically negative for estrogen receptor, progesterone receptor, and ErbB2 (due to deletion or lack of amplification). No dominant proliferative driver has been identified for this type of cancer, and effective targeted therapy is lacking. In this study, we hypothesized that triple negative breast cancer cells are multi-driver cancer cells, and evaluated a biphasic mathematical model for identifying potent and synergistic drug combinations for multi-driver cancer cells. The responses of two triple negative breast cancer cell lines, MDA-MB-231 and MDA-MB-468, to a panel of targeted therapy drugs were determined over a broad range of concentrations. The analyses of the drug responses by the biphasic mathematical model revealed that both cell lines were indeed dependent on multiple drivers, and inhibitors of individual drivers caused a biphasic response: a target-specific partial inhibition at low nM concentrations, and an off-target toxicity at μM concentrations. We further demonstrated that combinations of drugs, targeting each driver, cause potent, synergistic, and cell-specific cell killing. Immunoblotting analysis of the effects of the individual drugs and drug combinations on the signaling pathways supports the above conclusion. These results support a multi-driver proliferation hypothesis for these triple negative breast cancer cells, and demonstrate the applicability of the biphasic mathematical model for identifying effective and synergistic targeted drug combinations for triple negative breast cancer cells.

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