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Computational Drug Discovery and Development Along With Their Applications in the Treatment of Women-Associated Cancers
Published in Shazia Rashid, Ankur Saxena, Sabia Rashid, Latest Advances in Diagnosis and Treatment of Women-Associated Cancers, 2022
Rahul Kumar, Rakesh Kumar, Harsh Goel, Somorjit Singh Ningombam, Pranay Tanwar
Expression profiles of a gene and protein enlighten the diversified pathways involved in the proliferation of the cells. PPI also play a direct role in some cancers. Likewise, cervical cancer is the acquired infection of HPV during the commencement of sexual activity. PPI studies reveal that the E6 and E7 proteins of virus interact with p53 and Rb of host proteins that results the progression of infected cells into malignant cells [13]. Likewise in breast cancer, overexpression of epidermal growth factor receptor in HER2+ subtype and estrogen receptor in luminal subtype facilitate the potential targets for its treatment. Apart from this, various pathways such as MAPK, PI3K, TGF-β, Notch, hedgehog, Wnt/β-catenin and Hippo signalling are involved in the conversion of normal breast cells into the breast cancer stem cells and help in acquire stemness phenotype [14].
Breast Cancer Stem Cells and Their Niche: Lethal Seeds in Lethal Soil
Published in Brian Leyland-Jones, Pharmacogenetics of Breast Cancer, 2020
Danuta Balicki, Brian Leyland-Jones, Max S. Wicha
Breast cancer stem cell markers and the critical molecules in the pathways that drive their self-renewal are necessary to complete the molecular portrait of breast cancer. Our failure to eradicate most cancers may be as fundamental as a misidentification of the target cancer stem cell (Fig. 3) (6). The fact that stem cells rarely divide and have unique cellular properties, coupled with the observation that they may have high levels of drug transporters to pump chemotherapy agents out of the cell, has led many to believe that traditional chemo- or radiation therapies are insufficient to clear these tumor-initiating cells from the body (92). Clinical observations indicate that breast cancer responses to therapy do not necessarily correlate with patient survival and are incomplete clinical endpoints. Instead, the effectiveness of these treatments should be evaluated by decreased cancer recurrence and metastases as measures of therapeutic efficacy (92). As the molecular pathways that govern normal and cancer stem cells overlap, the targeting of these pathways could have harmful effects on the homeostatic function of normal stem cells. Targeted therapies that specifically eliminate cancer stem cells could further revolutionize the ways by which we treat cancer.
Dietary Phytochemicals as a Potential Source for Targeting Cancer Stem Cells
Published in Cancer Investigation, 2021
Prasath Manogaran, Devan Umapathy, Manochitra Karthikeyan, Karthikkumar Venkatachalam, Anbu Singaravelu
Past studies have documented that breast cancer stem cells are responsible for the failure of therapeutic intervention (58). By contrast, a recent study estimated that about 72% of women were inherited by harmful BRCA1 mutation and it served as a mammary stem cell fate determinant (59). However, defective BRCA1 cancer cells were difficult for prognosis and diagnosis. Hence, there is an urgent need to identify the surface marker to diagnose defective BRCA1 cancer and also to identify the natural molecule to suppress these cancer stem cell markers which could be the novel therapy for cancer (60,61) and they found positive ALDH1 expression is the best biomarker to diagnose BRCA1-defective breast cancer cells, treatment of plumbagin to ALDH1 positive cells induces the ROS mediated apoptosis mode of cell death (60). Apart from that plumbagin treatment inhibits the BRCA1/2 silence prostate cancer cells by modulating mitochondrial membrane potential that leads to the activation of caspase 8, caspase 9, and caspase 3 molecules. Therefore, plumbagin treatment may decrease the cancer stem cell marker (CD133 & CD44) and sphere formation ability (61) (Figure 3).
Radiation induces an inflammatory response that results in STAT3-dependent changes in cellular plasticity and radioresistance of breast cancer stem-like cells
Published in International Journal of Radiation Biology, 2020
Kimberly M. Arnold, Lynn M. Opdenaker, Nicole J. Flynn, Daniel Kwesi Appeah, Jennifer Sims-Mourtada
Growing evidence suggests that treatment-resistant breast cancer stem cells are responsible for tumor growth, recurrence, and metastasis, however, how these cells evade treatment is unclear. The IL-6 STAT3 pathway has been shown to promote growth of cancer stem cells in many solid tumors (Lee et al. 2011). Additionally, STAT3 activation within the tumor has been shown to promote an immunosuppressive microenvironment. Targeted deletion of STAT3 in the PyVmT mammary tumor model lead to increased immune infiltration and regression of early breast cancer lesions (Jones et al. 2016). Furthermore, sustained STAT3 activation in tumor cells contributes to release of immunosuppressive factors such as IL-10 and IL-6 which promote expansion regulatory T cells and myeloid-derived suppressor cells (Lee et al. 2011; Su et al. 2018). Although radiation has been shown to promote priming of T-cell responses in some cases (Arnold et al. 2018), the role of radiation-induced IL-6 Stat3 signaling on the tumor microenvironment is unclear. However, targeting IL-6/STAT3 may lead to anti-tumor effects on both tumor and infiltrating immune cells, leading to reduced populations of resistant stem-like cells, and enhanced radiation induced immune responses.
Nanocarrier based approaches for targeting breast cancer stem cells
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2018
Sai Kiran S. S. Pindiprolu, Praveen T. Krishnamurthy, Pavan Kumar Chintamaneni, Veera Venkata Satyanarayana Reddy Karri
Breast cancer is the most frequently diagnosed cancer and is the second leading cause of cancer deaths in women. Metastasis and relapse of tumour are emerging as major challenges in treatment of breast cancer [1,2]. Compelling body of evidences suggests that, small population of tumour initiating cells within tumours called breast cancer stem cells (BCSCs) are responsible for tumour relapse and metastasis [3–6]. The quiescence, expression of higher levels of drug efflux transporters and high DNA repair capacity of BCSCs makes them to resist apoptosis by chemotherapeutic agents [7,8]. The pool of BCSCs which are spared after chemotherapy will convert into tumour cells in future and results in tumour relapse [9]. In addition, BCSCs promote metastasis by induction epithelial-to-mesenchymal transition (EMT), in which, epithelial cells lose their intercellular adhesion, accompanied by gain of invasive and migratory properties, which is a pre-requisite for metastasis [10–13] (Figure 1). It is, therefore, necessary to eradicate BCSCs to achieve radical cure in breast cancer.