Understanding Molecular Process and Chemotherapeutics for the Management of Breast Cancer.

2020 ◽  
Vol 14 ◽  
Author(s):  
Abhishek Kumar ◽  
Neeraj Masand ◽  
Vaishali M. Patil
Keyword(s):  
Breast Cancer ◽  
Molecular Mechanisms ◽  
Molecular Targets ◽  
Molecular Classification ◽  
Neoplastic Disease ◽  
Molecular Process ◽  
The Past ◽  
Anti Cancer ◽  
Molecular Etiology ◽  
Near Future

Abstract: Breast cancer is the most common and highly heterogeneous neoplastic disease comprised of several subtypes with distinct molecular etiology and clinical behaviours. The mortality observed over the past few decades and the failure in eradicating the disease is due to the lack of specific etiology, molecular mechanisms involved in initiation and progression of breast cancer. Understanding of the molecular classes of breast cancer may also lead to new biological insights and eventually to better therapies. The promising therapeutic targets and novel anti-cancer approaches emerging from these molecular targets that could be applied clinically in the near future are being highlighted. In addition, this review discusses some of the details of current molecular classification and available chemotherapeutics

Novel Findings of Anti-cancer Property of Propofol

2018 ◽  
Vol 18 (2) ◽  
pp. 156-165 ◽  
Author(s):  
Jiaqiang Wang ◽  
Chien-shan Cheng ◽  
Yan Lu ◽  
Xiaowei Ding ◽  
Minmin Zhu ◽  
...  
Keyword(s):  
General Anesthesia ◽  
Cancer Progression ◽  
Molecular Mechanisms ◽  
Intravenous Anesthetic ◽  
The Past ◽  
Anti Cancer ◽  
Underlying Mechanisms ◽  
Recent Attention

Background: Propofol, a widely used intravenous anesthetic agent, is traditionally applied for sedation and general anesthesia. Explanation: Recent attention has been drawn to explore the effect and mechanisms of propofol against cancer progression in vitro and in vivo. Specifically, the proliferation-inhibiting and apoptosis-inducing properties of propofol in cancer have been studied. However, the underlying mechanisms remain unclear. Conclusion: This review focused on the findings within the past ten years and aimed to provide a general overview of propofol's malignance-modulating properties and the potential molecular mechanisms.

scholarly journals The Evolving Role of Ferroptosis in Breast Cancer: Translational Implications Present and Future

Cancers ◽  
2021 ◽  
Vol 13 (18) ◽  
pp. 4576
Author(s):  
Hung-Yu Lin ◽  
Hui-Wen Ho ◽  
Yen-Hsiang Chang ◽  
Chun-Jui Wei ◽  
Pei-Yi Chu
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Regulatory Networks ◽  
Molecular Mechanisms ◽  
Drug Resistant ◽  
Therapeutic Targeting ◽  
The Past ◽  
Regulated Cell Death ◽  
Common Malignancy

Breast cancer (BC) is the most common malignancy among women worldwide. The discovery of regulated cell death processes has enabled advances in the treatment of BC. In the past decade, ferroptosis, a new form of iron-dependent regulated cell death caused by excessive lipid peroxidation has been implicated in the development and therapeutic responses of BC. Intriguingly, the induction of ferroptosis acts to suppress conventional therapy-resistant cells, and to potentiate the effects of immunotherapy. As such, pharmacological or genetic modulation targeting ferroptosis holds great potential for the treatment of drug-resistant cancers. In this review, we present a critical analysis of the current understanding of the molecular mechanisms and regulatory networks involved in ferroptosis, the potential physiological functions of ferroptosis in tumor suppression, its potential in therapeutic targeting, and explore recent advances in the development of therapeutic strategies for BC.

Chemopreventive Properties of Tolfenamic Acid: A Mechanistic Review

2018 ◽  
Vol 25 (14) ◽  
pp. 1598-1608 ◽  
Author(s):  
David Feldman ◽  
Elizabeth Leahy ◽  
Seong-Ho Lee
Keyword(s):  
Therapeutic Strategy ◽  
Molecular Mechanisms ◽  
Growth Arrest ◽  
Molecular Targets ◽  
Tolfenamic Acid ◽  
Research Groups ◽  
Cancer Hallmarks ◽  
Cancer Models ◽  
Anti Cancer ◽  
Inflammatory Drugs

Tolfenamic acid is one of the conventional non-steroidal anti-inflammatory drugs (NSAIDs) commonly used for the treatment of inflammation, migraines and pain. There has been a growing body of experimental evidence that tolfenamic acid possesses anti-cancer activity. However, in order to develop a therapeutic strategy using tolfenamic acid for the treatment of cancer, further research is required to highlight reliable cellular and molecular mechanisms of anti-cancer properties. Tolfenamic acid has been shown to alter the expression of several genes that represent cancer hallmarks including apoptosis, growth arrest, angiogenesis and metastasis. Recently, a couple of research groups including ours reported that tolfenamic acid targets multiple oncogenic or tumor suppressive signaling pathways in various types of cancer models. Here, we highlight multiple molecular targets responsible for the anti-cancer mechanism of tolfenamic acid and the benefits of combinational use of this drug with other anti-cancer drugs.

scholarly journals The Anti-Cancer Effect of Polyphenols against Breast Cancer and Cancer Stem Cells: Molecular Mechanisms

Nutrients ◽  
2016 ◽  
Vol 8 (9) ◽  
pp. 581 ◽  
Author(s):  
Ahmed Abdal Dayem ◽  
Hye Choi ◽  
Gwang-Mo Yang ◽  
Kyeongseok Kim ◽  
Subbroto Saha ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Stem Cells ◽  
Cancer Stem Cells ◽  
Molecular Mechanisms ◽  
Anti Cancer

scholarly journals Emerging anti-cancer molecular mechanisms of aminobisphosphonates

2006 ◽  
Vol 13 (1) ◽  
pp. 7-26 ◽  
Author(s):  
Michele Caraglia ◽  
Daniele Santini ◽  
Monica Marra ◽  
Bruno Vincenzi ◽  
Giuseppe Tonini ◽  
...  
Keyword(s):  
Bone Metastases ◽  
Clinical Studies ◽  
Molecular Mechanisms ◽  
Molecular Targets ◽  
Anti Cancer ◽  
Ras Family ◽  
Skeletal Related Events ◽  
Breast And Prostate Cancer ◽  
Related Proteins

Bone metastases are common in patients with many types of cancer, especially breast and prostate cancer — in which the incidence is approximately 70% among patients with advanced metastatic disease. Aminobisphosphonates (NBPs) have entered clinical practice in the treatment of bone metastases from several neoplasms, including breast and prostate adenocarcinoma, as a result of their anti-resorption properties. However, evidence has accumulated on the direct anti-tumour effects of NBPs. This review describes the metabolic pathways that are putative molecular targets of NBPs and that are involved in the prenylation processes of several intracellular small GTP-binding proteins (ras family related proteins). The latter regulate the intracellular survival and proliferative pathways of tumour cells and could be the intracellular molecular targets of the NBPs responsible for the direct anti-cancer effects, even if definitive conclusions cannot be drawn at present. Different mechanisms have been reported to account for the anti-neoplastic action of NBPs, including: the induction of apoptosis; cell cycle perturbations; and anti-invasive, anti-migration and anti-angiogenic effects. Moreover, this review describes the most important clinical studies that demonstrate the activity of NBPs in preventing skeletal-related events induced by bone metastases. The main pharmacokinetic pitfalls of NBPs are described, and methods of overcoming these pitfalls through the use of liposome vehicles are proposed. Finally, the principal pre-clinical studies on the interaction between NBPs and other biological agents are also described; these studies may enable reductions in the in vivo NBP concentrations required to achieve anti-tumour activity. To date, however, the real molecular targets of NBPs are not completely known and new technological platforms are required in order to detect them and to develop new anti-cancer strategies based on the use of NBPs.

scholarly journals Anti-Hepatocellular Carcinoma Biomolecules: Molecular Targets Insights

2021 ◽  
Vol 22 (19) ◽  
pp. 10774
Author(s):  
Nouf Juaid ◽  
Amr Amin ◽  
Ali Abdalla ◽  
Kevin Reese ◽  
Zaenah Alamri ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Molecular Mechanisms ◽  
Treatment Strategies ◽  
Molecular Targets ◽  
Quantitative Structure Activity Relationship ◽  
Efficient Treatment ◽  
Signaling Mechanisms ◽  
Anti Cancer ◽  
Therapeutic Molecules ◽  
Essential Resource

This report explores the available curative molecules directed against hepatocellular carcinoma (HCC). Limited efficiency as well as other drawbacks of existing molecules led to the search for promising potential alternatives. Understanding of the cell signaling mechanisms propelling carcinogenesis and driven by cell proliferation, invasion, and angiogenesis can offer valuable information for the investigation of efficient treatment strategies. The complexity of the mechanisms behind carcinogenesis inspires researchers to explore the ability of various biomolecules to target specific pathways. Natural components occurring mainly in food and medicinal plants, are considered an essential resource for discovering new and promising therapeutic molecules. Novel biomolecules normally have an advantage in terms of biosafety. They are also widely diverse and often possess potent antioxidant, anti-inflammatory, and anti-cancer properties. Based on quantitative structure–activity relationship studies, biomolecules can be used as templates for chemical modifications that improve efficiency, safety, and bioavailability. In this review, we focus on anti-HCC biomolecules that have their molecular targets partially or completely characterized as well as having anti-cancer molecular mechanisms that are fairly described.

Transcriptome Analysis of MDA-MB-231 Cells Treated with Fumosorinone Isolated from Insect Pathogenic Fungi

2020 ◽  
Vol 20 (4) ◽  
pp. 417-428
Author(s):  
Zhiqin Liu ◽  
Yingchao Tian ◽  
Queting Chen ◽  
Gaotao Zhang ◽  
Chunqing Li ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Molecular Mechanisms ◽  
Pathogenic Fungi ◽  
Migration And Invasion ◽  
Receptor Interaction ◽  
Cancer Cell Growth ◽  
Qrt Pcr ◽  
Insect Pathogenic Fungi ◽  
Anti Cancer

Background: In our previous study, we have isolated a new compound, named Fumosorinone (FU) from insect pathogenic fungi, and was found to inhibit proliferation, migration, and invasion of breast cancer MDA-MB-231 cells. Objective: The aim of this study was to identify the underlying molecular mechanisms for FU effects on MDAMB- 231 cells. Methods: After MDA-MB-231 cells were treated with FU for 48h, RNA sequencing was used to identify the effect of FU on the transcriptome of MDA-MB-231 cells. The validation of the relative expression of the selective genes was done using quantitative real-time PCR (qRT-PCR). Results: The transcriptome results showed that 2733 genes were differentially expressed between the untreated and the FU-treated cells, including 1614 up-regulated and 1119 down-regulated genes. The multiple genes are associated with cancer cell growth, migration, and invasion. Functional analysis identified multitude of pathways related to cancer, such as cell cycle, ECM–receptor interaction, p53 signaling pathway. We selected 4 upregulated and 9 downregulated genes, which are associated with breast cancer to verify their expression using qRT-PCR. The validation showed that HSD3B1, ALOX5, AQP5, COL1A2, CCNB1, CCND1, VCAM-1, PTPN1 and PTPN11 were significantly downregulated while DUSP1, DUSP5, GADD45A, EGR1 were upregulated in FU-treated MDA-MB-231cells. Conclusion: These aberrantly expressed genes and pathways may play pivotal roles in the anti-cancer activity of FU, and maybe potential targets of FU treatments for TNBC. Further investigations are required to evaluate the FU mechanisms of anti-cancer action in vivo.

scholarly journals Improving Cancer Immunotherapy by Targeting the Hypoxic Tumor Microenvironment: New Opportunities and Challenges

Cells ◽  
2019 ◽  
Vol 8 (9) ◽  
pp. 1083 ◽  
Author(s):  
Muhammad Zaeem Noman ◽  
Meriem Hasmim ◽  
Audrey Lequeux ◽  
Malina Xiao ◽  
Caroline Duhem ◽  
...  
Keyword(s):  
Tumor Microenvironment ◽  
Molecular Mechanisms ◽  
Cancer Therapies ◽  
Hallmarks Of Cancer ◽  
The Past ◽  
Therapeutic Value ◽  
Anti Cancer ◽  
Microenvironmental Factors ◽  
Hypoxic Tumor ◽  
Insight Into

Initially believed to be a disease of deregulated cellular and genetic expression, cancer is now also considered a disease of the tumor microenvironment. Over the past two decades, significant and rapid progress has been made to understand the complexity of the tumor microenvironment and its contribution to shaping the response to various anti-cancer therapies, including immunotherapy. Nevertheless, it has become clear that the tumor microenvironment is one of the main hallmarks of cancer. Therefore, a major challenge is to identify key druggable factors and pathways in the tumor microenvironment that can be manipulated to improve the efficacy of current cancer therapies. Among the different tumor microenvironmental factors, this review will focus on hypoxia as a key process that evolved in the tumor microenvironment. We will briefly describe our current understanding of the molecular mechanisms by which hypoxia negatively affects tumor immunity and shapes the anti-tumor immune response. We believe that such understanding will provide insight into the therapeutic value of targeting hypoxia and assist in the design of innovative combination approaches to improve the efficacy of current cancer therapies, including immunotherapy.

scholarly journals The Anticancer Effects of FDI-6, a FOXM1 Inhibitor, on Triple Negative Breast Cancer

2021 ◽  
Vol 22 (13) ◽  
pp. 6685
Author(s):  
Karan Ulhaka ◽  
Kanyanatt Kanokwiroon ◽  
Mattaka Khongkow ◽  
Rassanee Bissanum ◽  
Thanaporn Khunpitak ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Triple Negative Breast Cancer ◽  
Molecular Mechanisms ◽  
Triple Negative ◽  
Significant Inhibition ◽  
Migration And Invasion ◽  
Sulforhodamine B ◽  
Anticancer Effects ◽  
Anti Cancer ◽  
Invasion Assays

Triple-negative breast cancer (TNBC) presents an important clinical challenge, as it does not respond to endocrine therapies or other available targeting agents. FOXM1, an oncogenic transcriptional factor, has reported to be upregulated and associated with poor clinical outcomes in TNBC patients. In this study, we investigated the anti-cancer effects of FDI-6, a FOXM1 inhibitor, as well as its molecular mechanisms, in TNBC cells. Two TNBC cell lines, MDA-MB-231 and HS578T, were used in this study. The anti-cancer activities of FDI-6 were evaluated using various 2D cell culture assays, including Sulforhodamine B (SRB), wound healing, and transwell invasion assays together with 3D spheroid assays, mimicking real tumour structural properties. After treatment with FDI-6, the TNBC cells displayed a significant inhibition in cell proliferation, migration, and invasion. Increased apoptosis was also observed in the treated cells. In addition, we found that FDI-6 lead to the downregulation of FOXM1 and its key oncogenic targets, including CyclinB1, Snail, and Slug. Interestingly, we also found that the FDI-6/Doxorubicin combination significantly enhanced the cytotoxicity and apoptotic properties, suggesting that FDI-6 might improve chemotherapy treatment efficacy and reduce unwanted side effects. Altogether, FDI-6 exhibited promising anti-tumour activities and could be developed as a newly effective treatment for TNBC.

scholarly journals Dll1+ quiescent tumor stem cells drive chemoresistance in breast cancer through NF-κB survival pathway

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Sushil Kumar ◽  
Ajeya Nandi ◽  
Snahlata Singh ◽  
Rohan Regulapati ◽  
Ning Li ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Patients ◽  
Molecular Mechanisms ◽  
Conditional Knockout ◽  
Cancer Resistance ◽  
Breast Cancer Patients ◽  
Notch Receptors ◽  
Survival Pathway ◽  
Tumor Growth And Metastasis ◽  
Near Future

AbstractDevelopment of chemoresistance in breast cancer patients greatly increases mortality. Thus, understanding mechanisms underlying breast cancer resistance to chemotherapy is of paramount importance to overcome this clinical challenge. Although activated Notch receptors have been associated with chemoresistance in cancer, the specific Notch ligands and their molecular mechanisms leading to chemoresistance in breast cancer remain elusive. Using conditional knockout and reporter mouse models, we demonstrate that tumor cells expressing the Notch ligand Dll1 is important for tumor growth and metastasis and bear similarities to tumor-initiating cancer cells (TICs) in breast cancer. RNA-seq and ATAC-seq using reporter models and patient data demonstrated that NF-κB activation is downstream of Dll1 and is associated with a chemoresistant phenotype. Finally, pharmacological blocking of Dll1 or NF-κB pathway completely sensitizes Dll1+ tumors to chemotherapy, highlighting therapeutic avenues for chemotherapy resistant breast cancer patients in the near future.

Sign in / Sign up

Export Citation Format

Share Document