scholarly journals Discrete signaling pathways participate in RB-dependent responses to chemotherapeutic agents

Oncogene ◽  
2004 ◽  
Vol 23 (23) ◽  
pp. 4107-4120 ◽  
Author(s):  
Christopher N Mayhew ◽  
Lisa M Perkin ◽  
Xiaoping Zhang ◽  
Julien Sage ◽  
Tyler Jacks ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Chemotherapeutic Agents

scholarly journals The Promise of Integrins as Effective Targets for Anticancer Agents

2002 ◽  
Vol 2 (3) ◽  
pp. 124-130 ◽  
Author(s):  
William L. Rust ◽  
Stephen W. Carper ◽  
George E. Plopper
Keyword(s):  
Monoclonal Antibodies ◽  
Drug Design ◽  
Cell Surface ◽  
Signaling Pathways ◽  
Anticancer Agents ◽  
Chemotherapeutic Agents ◽  
Migration And Invasion ◽  
Chemotherapeutic Drug ◽  
Cellular Processes ◽  
Adenovirus Vectors

This review will briefly describe integrin function, address why integrins are attractive targets for chemotherapeutic drug design, and discuss some ongoing studies aimed at inhibiting integrin activity. Integrins are cell surface heterodimeric receptors. They modulate many cellular processes including: growth, death (apoptosis), adhesion, migration, and invasion by activating several signaling pathways. Many potential chemotherapeutic agents target integrins directly (eg, polypeptides, monoclonal antibodies, adenovirus vectors). These agents may be clinically useful in controlling the metastatic spread of cancer.

scholarly journals Natural Products Targeting Cancer Stem Cells for Augmenting Cancer Therapeutics

2021 ◽  
Vol 22 (23) ◽  
pp. 13044
Author(s):  
Ari Meerson ◽  
Soliman Khatib ◽  
Jamal Mahajna
Keyword(s):  
Stem Cells ◽  
Natural Products ◽  
Cancer Stem Cells ◽  
Signaling Pathways ◽  
Tumor Cells ◽  
Cancer Therapeutics ◽  
Chemotherapeutic Agents ◽  
Biologically Active ◽  
Approved Drugs ◽  
Multiple Signaling

Cancer stem cells (CSC) have been identified in several types of solid tumors. In some cases, CSC may be the source of all the tumor cells, the cause of the tumor’s resistance to chemotherapeutic agents, and the source of metastatic cells. Thus, a combination therapy targeting non-CSC tumor cells as well as specifically targeting CSCs holds the potential to be highly effective. Natural products (NPs) have been a historically rich source of biologically active compounds and are known for their ability to influence multiple signaling pathways simultaneously with negligible side effects. In this review, we discuss the potential of NPs in targeting multiple signaling pathways in CSC and their potential to augment the efficacy of standard cancer therapy. Specifically, we focus on the anti-CSC activities of flavonoids, FDA-approved drugs originating from natural sources. Additionally, we emphasize the potential of NPs in targeting microRNA-mediated signaling, given the roles of microRNA in the maintenance of the CSC phenotype.

scholarly journals The Multi-Omic Prognostic Model of Oxidative Stress-Related Genes in Acute Myeloid Leukemia

2021 ◽  
Vol 12 ◽  
Author(s):  
Chao Dong ◽  
Naijin Zhang ◽  
Lijun Zhang
Keyword(s):  
Oxidative Stress ◽  
Acute Myeloid Leukemia ◽  
Signaling Pathways ◽  
Myeloid Leukemia ◽  
Risk Model ◽  
Enrichment Analysis ◽  
Chemotherapeutic Agents ◽  
The Cancer Genome Atlas ◽  
Stress Genes ◽  
Acute Myeloid

Background: Acute myeloid leukemia (AML) is one of the most common cancers in the world, and oxidative stress is closely related to leukemia. A lot of effort has been made to improve the prognosis of AML. However, the situation remains serious. Hence, we focused on the study of prognostic genes in AML.Materials and Methods: Prognostic oxidative stress genes were screened out. The gene expression profile of AML patients was downloaded from the The Cancer Genome Atlas (TCGA) database. The oxidative stress-related model was constructed, by which the prognosis of AML patients was predicted using the two GEO GSE23143 datasets and the stability of the GSE71014 authentication model.Results: The prognostic oxidative stress genes were screened out in AML, and the prognostic genes were significantly enriched in a large number of pathways based on Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis. There was a complex interaction between prognostic genes and transcription factors. After constructing the prediction model, the clinical predictive value of the model was discussed in a multi-omic study. We investigated the sensitivity of risk score to common chemotherapeutic agents, the influence of signaling pathways on the prognosis of AML patients, and the correlation of multiple genes with immune score and immune dysfunction.Conclusions: A highly effective prognostic risk model for AML patients was established and validated. The association of prognostic oxidative stress genes with drug sensitivity, signaling pathways, and immune infiltration was explored. The results suggested that oxidative stress genes promised to be potential prognostic biomarkers for AML, which may provide a new basis for disease management.

Selective targeting of cancer signaling pathways with nanomedicines: challenges and progress

2020 ◽  
Vol 16 (35) ◽  
pp. 2959-2979 ◽  
Author(s):  
Harshita Abul Barkat ◽  
Sabya Sachi Das ◽  
Md Abul Barkat ◽  
Sarwar Beg ◽  
Hazrina Ab Hadi
Keyword(s):  
Signaling Pathways ◽  
Tumor Targeting ◽  
Causes Of Death ◽  
Therapeutic Agents ◽  
Chemotherapeutic Agents ◽  
Cancer Therapies ◽  
Molecular Signaling ◽  
Cancer Management ◽  
Selective Targeting ◽  
The Right

Cancer is one of the leading causes of death worldwide. Regardless of advances in understanding the molecular mechanics of cancer, its treatment is still lacking and the death rates for many forms of the disease remain the same as six decades ago. Although a variety of therapeutic agents and strategies have been reported, these therapies often failed to provide efficient therapy to patients as a consequence of the inability to deliver right and adequate chemotherapeutic agents to the right place. However, the situation has started to revolutionize substantially with the advent of novel ‘targeted’ nanocarrier-based cancer therapies. Such therapies hold great potential in cancer management as they are biocompatible, tailored to specific needs, tolerated and deliver enough drugs at the targeted site. Their use also enhances the delivery of chemotherapeutics by improving biodistribution, lowering toxicity, inhibiting degradation and increasing cellular uptake. However, in some instances, nonselective targeting is not enough and the inclusion of a ligand moiety is required to achieve tumor targeting and enhanced drug accumulation at the tumor site. This contemporary review outlines the targeting potential of nanocarriers, highlighting the essentiality of nanoparticles, tumor-associated molecular signaling pathways, and various biological and pathophysiological barriers.

scholarly journals Wnt/β-catenin signaling as an emerging potential key pharmacological target in cholangiocarcinoma

2020 ◽  
Vol 40 (3) ◽  
Author(s):  
Guo-Feng Zhang ◽  
Ling Qiu ◽  
Shu-Li Yang ◽  
Jia-Cheng Wu ◽  
Tong-Jun Liu
Keyword(s):  
Signaling Pathways ◽  
Nuclear Translocation ◽  
Efflux Pump ◽  
Multidrug Resistant ◽  
Chemotherapeutic Agents ◽  
Regulatory Subunit ◽  
Wnt Ligands ◽  
Liver Kinase B1 ◽  
Gsk 3Β

Abstract Cholangiocarcinoma (CCA) is a fatal malignant tumor of biliary epithelial cells involving intra- or extra-hepatic bile ducts. The prognosis of CCA is generally poor due to its diagnosis at the late stages. The currently employed chemotherapeutic agents do not increase the survival rate in patients with unresectable CCA. Accordingly, there is a need to identify new therapeutic agents for the effective management of intra- and extra-hepatic CCA. Clinical as well as preclinical studies have suggested the key role of the activation of Wnt/β-catenin signaling pathway in the induction and progression of CCA. There is an up-regulation of different Wnt ligands including Wnt2, Wnt3, Wnt5, Wnt7 and Wnt10 along with redistribution of β-catenin (more expression in the nucleus and lesser on the cell surface due to nuclear translocation of β-catenin) in different types of malignant biliary tumors. Apart from the role of this pathway in the induction and progression of CCA, this pathway is also involved in inducing multidrug resistance by inducing the expression of P-glycoprotein efflux pump on the cancer cells. These deleterious effects of Wnt/β-catenin signaling are mediated in association with other signaling pathways involving microRNAs (miRNAs), PI3K/AKT/PTEN/GSK-3β, retinoic acid receptors (RARs), dickkopf-1 (DKK1), protein kinase A regulatory subunit 1 α (PRKAR1A/PKAI), (SLAP), liver kinase B1 (LKB1) and CXCR4. The selective inhibitors of Wnt/β-catenin signaling may be potentially employed to overcome multidrug-resistant, fatal CCA. The present review discusses the role of Wnt/β-catenin along with its relation with other signaling pathways in the induction and progression of CCA.

scholarly journals MicroRNAs as the critical regulators of cisplatin resistance in gastric tumor cells

2021 ◽  
Vol 43 (1) ◽  
Author(s):  
Amir Sadra Zangouei ◽  
Meysam Moghbeli
Keyword(s):  
Signaling Pathways ◽  
Tumor Cells ◽  
Molecular Mechanisms ◽  
Target Genes ◽  
Cisplatin Resistance ◽  
Chemotherapeutic Agents ◽  
High Rate ◽  
Gastric Tumor ◽  
High Dose ◽  
Mesenchymal Transition

AbstractCombined chemotherapeutic treatment is the method of choice for advanced and metastatic gastric tumors. However, resistance to chemotherapeutic agents is one of the main challenges for the efficient gastric cancer (GC) treatment. Cisplatin (CDDP) is used as an important regimen of chemotherapy for GC which induces cytotoxicity by interfering with DNA replication in cancer cells and inducing their apoptosis. Majority of patients experience cisplatin-resistance which is correlated with tumor metastasis and relapse. Moreover, prolonged and high-dose cisplatin administrations cause serious side effects such as nephrotoxicity, ototoxicity, and anemia. Since, there is a high rate of recurrence after CDDP treatment in GC patients; it is required to clarify the molecular mechanisms associated with CDDP resistance to introduce novel therapeutic methods. There are various cell and molecular processes associated with multidrug resistance (MDR) including drug efflux, detoxification, DNA repair ability, apoptosis alteration, signaling pathways, and epithelial-mesenchymal transition (EMT). MicroRNAs are a class of endogenous non-coding RNAs involved in chemo resistance of GC cells through regulation of all of the MDR mechanisms. In present review we have summarized all of the miRNAs associated with cisplatin resistance based on their target genes and molecular mechanisms in gastric tumor cells. This review paves the way of introducing a miRNA-based panel of prognostic markers to improve the efficacy of chemotherapy and clinical outcomes in GC patients. It was observed that miRNAs are mainly involved in cisplatin response of gastric tumor cells via regulation of signaling pathways, autophagy, and apoptosis.

Exploring Signaling Pathways and Pancreatic Cancer Treatment Approaches Using Genetic Models

2019 ◽  
Vol 19 (14) ◽  
pp. 1112-1125
Author(s):  
Shorooq Khader ◽  
Anita Thyagarajan ◽  
Ravi P. Sahu
Keyword(s):  
Pancreatic Cancer ◽  
Signaling Pathways ◽  
Treatment Options ◽  
Survival Rates ◽  
Genetic Alterations ◽  
Chemotherapeutic Agents ◽  
Genetic Models ◽  
Treatment Approaches ◽  
Regulatory Pathways ◽  
The Impact

Despite available treatment options, the overall survival rates of pancreatic cancer patients remain dismal. Multiple counter-regulatory pathways have been identified and shown to be involved in interfering with the efficacy of therapeutic agents. In addition, various known genetic alterations in the cellular signaling pathways have been implicated in affecting the growth and progression of pancreatic cancer. Nevertheless, the significance of other unknown pathways is yet to be explored, which provides the rationale for the intervention of new approaches. Several experimental genetic models have been explored to define the impact of key signaling cascades, and their mechanisms in the pathophysiology as well as treatment approaches of pancreatic cancer. The current review highlights the recent updates, and significance of such genetic models in the therapeutic efficacy of anti-tumor agents including the standard chemotherapeutic agents, natural products, cell signaling inhibitors, immunebased therapies and the combination of these approaches in pancreatic cancer.

Curcumin mediates anticancer effects by modulating multiple cell signaling pathways

2017 ◽  
Vol 131 (15) ◽  
pp. 1781-1799 ◽  
Author(s):  
Ajaikumar B. Kunnumakkara ◽  
Devivasha Bordoloi ◽  
Choudhary Harsha ◽  
Kishore Banik ◽  
Subash C. Gupta ◽  
...  
Keyword(s):  
Cell Signaling ◽  
Signaling Pathways ◽  
Curcuma Longa ◽  
Chemotherapeutic Agents ◽  
Clinical Findings ◽  
Anticancer Activities ◽  
Antibacterial And Antifungal Activities ◽  
Multiple Cell ◽  
Approved Drugs ◽  
Cell Signaling Pathways

Curcumin, a component of a spice native to India, was first isolated in 1815 by Vogel and Pelletier from the rhizomes of Curcuma longa (turmeric) and, subsequently, the chemical structure of curcumin as diferuloylmethane was reported by Milobedzka et al. [(1910) 43., 2163-2170]. Since then, this polyphenol has been shown to exhibit antioxidant, anti-inflammatory, anticancer, antiviral, antibacterial, and antifungal activities. The current review primarily focuses on the anticancer potential of curcumin through the modulation of multiple cell signaling pathways. Curcumin modulates diverse transcription factors, inflammatory cytokines, enzymes, kinases, growth factors, receptors, and various other proteins with an affinity ranging from the pM to the mM range. Furthermore, curcumin effectively regulates tumor cell growth via modulation of numerous cell signaling pathways and potentiates the effect of chemotherapeutic agents and radiation against cancer. Curcumin can interact with most of the targets that are modulated by FDA-approved drugs for cancer therapy. The focus of this review is to discuss the molecular basis for the anticancer activities of curcumin based on preclinical and clinical findings.

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