Role of Nitric Oxide for Modulation of Cancer Therapy Resistance

2010 ◽  
pp. 265-282
Author(s):  
Thomas Efferth
Keyword(s):  
Nitric Oxide ◽  
Cancer Therapy ◽  
Therapy Resistance

scholarly journals Cell Plasticity and Prostate Cancer: The Role of Epithelial–Mesenchymal Transition in Tumor Progression, Invasion, Metastasis and Cancer Therapy Resistance

Cancers ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 2795
Author(s):  
Sofia Papanikolaou ◽  
Aikaterini Vourda ◽  
Spyros Syggelos ◽  
Kostis Gyftopoulos
Keyword(s):  
Prostate Cancer ◽  
Cancer Therapy ◽  
Tumor Progression ◽  
Epithelial Mesenchymal Transition ◽  
Metastatic Tumor ◽  
Therapy Resistance ◽  
Cellular Process ◽  
Cell Plasticity ◽  
Mesenchymal Transition

Prostate cancer, the second most common malignancy in men, is characterized by high heterogeneity that poses several therapeutic challenges. Epithelial–mesenchymal transition (EMT) is a dynamic, reversible cellular process which is essential in normal embryonic morphogenesis and wound healing. However, the cellular changes that are induced by EMT suggest that it may also play a central role in tumor progression, invasion, metastasis, and resistance to current therapeutic options. These changes include enhanced motility and loss of cell–cell adhesion that form a more aggressive cellular phenotype. Moreover, the reverse process (MET) is a necessary element of the metastatic tumor process. It is highly probable that this cell plasticity reflects a hybrid state between epithelial and mesenchymal status. In this review, we describe the underlying key mechanisms of the EMT-induced phenotype modulation that contribute to prostate tumor aggressiveness and cancer therapy resistance, in an effort to provide a framework of this complex cellular process.

scholarly journals The role of lineage plasticity in prostate cancer therapy resistance

2019 ◽  
pp. clincanres.1423.2019 ◽  
Author(s):  
Himisha Beltran ◽  
Andrew Hruszkewycz ◽  
Howard I. Scher ◽  
Jeffrey Hildesheim ◽  
Jennifer Isaacs ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Therapy ◽  
Therapy Resistance ◽  
Prostate Cancer Therapy

Role of toll-like receptor 3 in prostate cancer therapy-resistance

2019 ◽  
Vol 18 (8) ◽  
pp. e3124
Author(s):  
X.M. Muresan ◽  
S. Drapela ◽  
E. Slabakova ◽  
J. Remsik ◽  
R. Fedr ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Therapy ◽  
Therapy Resistance ◽  
Toll Like Receptor ◽  
Prostate Cancer Therapy

scholarly journals MiR-141 Activates Nrf2-Dependent Antioxidant Pathway via Down-Regulating the Expression of Keap1 Conferring the Resistance of Hepatocellular Carcinoma Cells to 5-Fluorouracil

2015 ◽  
Vol 35 (6) ◽  
pp. 2333-2348 ◽  
Author(s):  
Liang Shi ◽  
Lili Wu ◽  
Zhanguo Chen ◽  
Jianrong Yang ◽  
Xiaofei Chen ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cancer Therapy ◽  
Nuclear Translocation ◽  
Therapy Resistance ◽  
Parental Cell ◽  
Significant Inhibition ◽  
Carcinoma Cells ◽  
Pcr Analysis ◽  
Hepatocellular Carcinoma Cells

Background: Hepatocellular carcinoma (HCC) is one of the most lethal malignancies worldwide. A major cause for the failure of cancer therapy is the development of chemoresistance. Although progress has been made in the study of the mechanisms underlying cancer cells resistance, little is known about the role of microRNAs (miRNAs) in cancer therapy resistance. Methods and Results: Fifteen miRNAs, including 6 up-regulated miRNAs (> 2.0-fold) and 9 down-regulated miRNAs (< 0.5-fold) were differentially expressed in 5-fluorouracil-resistant and their parental cell-lines (HepG2, HepG2/5-FU) by miRNA microarrays. Microarray results were confirmed by validating quantitative real-time polymerase chain reaction (qRT-PCR) analysis. Up-regulation of miR-141 expression resulted in a significant inhibition of 5-FU-mediated cytotoxicity and apoptosis in various hepatocellular carcinoma cells-lines. Mechanically, miR-141 promoted Kelch-like ECH-associated protein 1 (Keap1) mRNA degradation by directly targeting the Keap1 3'untranslated region (3'UTR). Treatment with miR-141 mimics in parental HepG2 cells, restored miR-141 expression and reduced Keap1 levels, thereby resulting in erythroid transcription factor NFE2-L2 (Nrf2) nuclear translocation, activation of Nrf2-dependent HO-1 gene transcription, and subsequent enhancement in 5-FU resistance. Conversely, restoring the expression of Keap1 partly recovered 5-FU sensitivity by counteracting miR-141-mediated 5-FU resistance. Conclusion: Our study showed that miR-141 plays a key role in 5-FU resistance by down-regulating Keap1 expression, thereby reactivating the Nrf2-dependent antioxidant pathway, which may serve as a potential target for overcoming 5-FU resistance in hepatocellular carcinoma cells.

scholarly journals Role of non-coding RNAs and RNA modifiers in cancer therapy resistance

2020 ◽  
Vol 19 (1) ◽  
Author(s):  
Xinyi Zhang ◽  
Kai Xie ◽  
Honghua Zhou ◽  
Yuwei Wu ◽  
Chan Li ◽  
...  
Keyword(s):  
Cancer Therapy ◽  
Therapy Resistance ◽  
Non Coding Rnas

scholarly journals Photodynamic Therapy with Zinc Phthalocyanine Inhibits the Stemness and Development of Colorectal Cancer: Time to Overcome the Challenging Barriers?

Molecules ◽  
2021 ◽  
Vol 26 (22) ◽  
pp. 6877
Author(s):  
Mahsa Gholizadeh ◽  
Mohammad Amin Doustvandi ◽  
Fateme Mohammadnejad ◽  
Mahdi Abdoli Shadbad ◽  
Habib Tajalli ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Photodynamic Therapy ◽  
Cancer Therapy ◽  
Therapy Resistance ◽  
Zinc Phthalocyanine ◽  
Apoptosis Pathway ◽  
Intrinsic Apoptosis Pathway ◽  
Sw480 Cells ◽  
Tumoral Cells

Photodynamic therapy (PDT) is a light-based cancer therapy approach that has shown promising results in treating various malignancies. Growing evidence indicates that cancer stem cells (CSCs) are implicated in tumor recurrence, metastasis, and cancer therapy resistance in colorectal cancer (CRC); thus, targeting these cells can ameliorate the prognosis of affected patients. Based on our bioinformatics results, SOX2 overexpression is significantly associated with inferior disease-specific survival and worsened the progression-free interval of CRC patients. Our results demonstrate that zinc phthalocyanine (ZnPc)-PDT with 12 J/cm2 or 24 J/cm2 irradiation can substantially decrease tumor migration via downregulating MMP9 and ROCK1 and inhibit the clonogenicity of SW480 cells via downregulating CD44 and SOX2. Despite inhibiting clonogenicity, ZnPc-PDT with 12 J/cm2 irradiation fails to downregulate CD44 expression in SW480 cells. Our results indicate that ZnPc-PDT with 12 J/cm2 or 24 J/cm2 irradiation can substantially reduce the cell viability of SW480 cells and stimulate autophagy in the tumoral cells. Moreover, our results show that ZnPc-PDT with 12 J/cm2 or 24 J/cm2 irradiation can substantially arrest the cell cycle at the sub-G1 level, stimulate the intrinsic apoptosis pathway via upregulating caspase-3 and caspase-9 and downregulating Bcl-2. Indeed, our bioinformatics results show considerable interactions between the studied CSC-related genes with the studied migration- and apoptosis-related genes. Collectively, the current study highlights the potential role of ZnPc-PDT in inhibiting stemness and CRC development, which can ameliorate the prognosis of CRC patients.

Abstract 693: Evaluating the role of CXCR2 receptor and its ligand in breast cancer therapy resistance

2011 ◽  
Author(s):  
Bhawna Sharma ◽  
Dhananjay M. Nawandar ◽  
Michelle L. Varney ◽  
Rakesh K. Singh
Keyword(s):  
Breast Cancer ◽  
Cancer Therapy ◽  
Therapy Resistance ◽  
Breast Cancer Therapy

scholarly journals Role of hypoxia in cancer therapy by regulating the tumor microenvironment

2019 ◽  
Vol 18 (1) ◽  
Author(s):  
Xinming Jing ◽  
Fengming Yang ◽  
Chuchu Shao ◽  
Ke Wei ◽  
Mengyan Xie ◽  
...  
Keyword(s):  
Dna Damage ◽  
Tumor Microenvironment ◽  
Cancer Therapy ◽  
Web Of Science ◽  
Therapy Resistance ◽  
Mitochondrial Activity ◽  
Cellular Expression ◽  
Clinical Resistance ◽  
Expression Program

Abstract Aim Clinical resistance is a complex phenomenon in major human cancers involving multifactorial mechanisms, and hypoxia is one of the key components that affect the cellular expression program and lead to therapy resistance. The present study aimed to summarize the role of hypoxia in cancer therapy by regulating the tumor microenvironment (TME) and to highlight the potential of hypoxia-targeted therapy. Methods Relevant published studies were retrieved from PubMed, Web of Science, and Embase using keywords such as hypoxia, cancer therapy, resistance, TME, cancer, apoptosis, DNA damage, autophagy, p53, and other similar terms. Results Recent studies have shown that hypoxia is associated with poor prognosis in patients by regulating the TME. It confers resistance to conventional therapies through a number of signaling pathways in apoptosis, autophagy, DNA damage, mitochondrial activity, p53, and drug efflux. Conclusion Hypoxia targeting might be relevant to overcome hypoxia-associated resistance in cancer treatment.

scholarly journals Specialized Pro-Resolving Mediators Mitigate Cancer-Related Inflammation: Role of Tumor-Associated Macrophages and Therapeutic Opportunities

2021 ◽  
Vol 12 ◽  
Author(s):  
Margot Lavy ◽  
Vanessa Gauttier ◽  
Nicolas Poirier ◽  
Sophie Barillé-Nion ◽  
Christophe Blanquart
Keyword(s):  
Cancer Therapy ◽  
Tumor Progression ◽  
Cancer Progression ◽  
Immune Escape ◽  
Therapy Resistance ◽  
High Plasticity ◽  
Tumor Cell Death ◽  
Tumor Associated Macrophages ◽  
Inflammation Resolution

Inflammation is a fundamental physiological response orchestrated by innate immune cells to restore tissue homeostasis. Specialized pro-resolving mediators (SPMs) are involved in active resolution of inflammation but when inflammation is incomplete, chronic inflammation creates a favorable environment that fuels carcinogenesis and cancer progression. Conventional cancer therapy also strengthens cancer-related inflammation by inducing massive tumor cell death that activate surrounding immune-infiltrating cells such as tumor-associated macrophages (TAMs). Macrophages are key actors of both inflammation and its active resolution due to their plastic phenotype. In line with this high plasticity, macrophages can be hijacked by cancer cells to support tumor progression and immune escape, or therapy resistance. Impaired resolution of cancer-associated inflammation supported by TAMs may thus reinforces tumor progression. From this perspective, recent evidence suggests that stimulating macrophage’s pro-resolving functions using SPMs can promote inflammation resolution in cancer and improve anticancer treatments. Thus, TAMs’ re-education toward an antitumor phenotype by using SPMs opens a new line of attack in cancer treatment. Here, we review SPMs’ anticancer capacities with special attention regarding their effects on TAMs. We further discuss how this new therapeutic approach could be envisioned in cancer therapy.

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