Role of 4-Thiazolidinone Scaffold in Targeting Variable Biomarkers and Pathways Involving Cancer

2021 ◽  
Vol 21 ◽  
Author(s):  
Meenakshi Negi ◽  
Pooja Chawla ◽  
Abdul Faruk ◽  
Viney Chawla
Keyword(s):  
Drug Resistance ◽  
Cancer Therapy ◽  
Cancer Progression ◽  
Cell Metabolism ◽  
Multi Drug Resistance ◽  
Treatment Scenario ◽  
Resistance Development ◽  
Normal Tissues ◽  
Colon Cancers ◽  
Transcriptional Changes

Background: Cancer can be considered as a genetic as well as a metabolic disorder. Current cancer treatment scenario looks like aggravating tumor cell metabolism, causing the disease to progress even with greater intensity. The cancer therapy is restricted to limitations of poor patient compliance due to toxicities to normal tissues and multi-drug resistance development. There is an emerging need for cancer therapy to be more focused on the better understanding of genetic, epigenetic and transcriptional changes resulting in cancer progression and their relationship with treatment sensitivity. Objective: The 4-thiazolidinone nucleus possesses marked anticancer potential towards different biotargets, thus targeting different cancer types like breast, prostate, lung, colorectal and colon cancers, renal cell adenocarcinomas and gliomas. Therefore, conjugating the 4-thiazolidinone scaffold with other promising moieties or by directing the therapy towards targeted drug delivery systems like the use of nanocarrier systems, can provide the gateway for optimizing the anticancer efficiency and minimizing the adverse effects and drug resistance development, thus providing stimulus for personalized pharmacotherapy. Methods: An exhaustive literature survey has been carried out to give an insight into the anticancer potential of the 4-thiazolidinone nucleus either alone or in conjugation with other active moieties, with the mechanisms involved in preventing proliferation and metastasis of cancer covering a vast range of publications of repute. Conclusion: This review aims to summarise the work reported on anticancer activity of 4-thiazolidinone derivatives covering various cancer biomarkers and pathways involved, citing the data from 2005 till now, which may be beneficial to the researchers for future development of more efficient 4-thiazolidinone derivatives.

scholarly journals Multi Drug Resistance in Cancer Therapy-An Overview

2019 ◽  
pp. 1-6 ◽  
Author(s):  
HARISH KADKOL ◽  
VIKAS JAIN ◽  
AMIT PATIL*
Keyword(s):  
Drug Resistance ◽  
Cancer Therapy ◽  
Multi Drug Resistance

scholarly journals MicroRNAs and Their Influence on the ZEB Family: Mechanistic Aspects and Therapeutic Applications in Cancer Therapy

Biomolecules ◽  
2020 ◽  
Vol 10 (7) ◽  
pp. 1040 ◽  
Author(s):  
Milad Ashrafizadeh ◽  
Hui Li Ang ◽  
Ebrahim Rahmani Moghadam ◽  
Shima Mohammadi ◽  
Vahideh Zarrin ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Cancer Therapy ◽  
Signaling Pathways ◽  
Tumor Cells ◽  
Cancer Progression ◽  
Epithelial Mesenchymal Transition ◽  
Migration And Invasion ◽  
Circular Rnas ◽  
Mesenchymal Transition ◽  
The Impact

Molecular signaling pathways involved in cancer have been intensively studied due to their crucial role in cancer cell growth and dissemination. Among them, zinc finger E-box binding homeobox-1 (ZEB1) and -2 (ZEB2) are molecules that play vital roles in signaling pathways to ensure the survival of tumor cells, particularly through enhancing cell proliferation, promoting cell migration and invasion, and triggering drug resistance. Importantly, ZEB proteins are regulated by microRNAs (miRs). In this review, we demonstrate the impact that miRs have on cancer therapy, through their targeting of ZEB proteins. MiRs are able to act as onco-suppressor factors and inhibit the malignancy of tumor cells through ZEB1/2 down-regulation. This can lead to an inhibition of epithelial-mesenchymal transition (EMT) mechanism, therefore reducing metastasis. Additionally, miRs are able to inhibit ZEB1/2-mediated drug resistance and immunosuppression. Additionally, we explore the upstream modulators of miRs such as long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs), as these regulators can influence the inhibitory effect of miRs on ZEB proteins and cancer progression.

scholarly journals LncRNA FEZF1-AS1 Promotes Multi-Drug Resistance of Gastric Cancer Cells via Upregulating ATG5

2021 ◽  
Vol 9 ◽  
Author(s):  
Zhifu Gui ◽  
Zhenguo Zhao ◽  
Qi Sun ◽  
Guoyi Shao ◽  
Jianming Huang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Drug Resistance ◽  
Cancer Progression ◽  
Molecular Mechanisms ◽  
Underlying Mechanism ◽  
Multi Drug Resistance ◽  
Gastric Cancer Cells ◽  
Poor Overall Survival

Long non-coding RNAs (lncRNAs) play important roles in human cancers including gastric cancer (GC). Dysregulation of lncRNAs is involved in a variety of pathological activities associated with gastric cancer progression and chemo-resistance. However, the role and molecular mechanisms of FEZF1-AS1 in chemoresistance of GC remain unknown. In this study, we aimed to determine the role of FEZF1-AS1 in chemoresistance of GC. The level of FEZF1-AS1 in GC tissues and GC cell lines was assessed by qRT-PCR. Our results showed that the expression of FEZF1-AS1 was higher in gastric cancer tissues than in adjacent normal tissues. Multivariate analysis identified that high level of FEZF1-AS1 is an independent predictor for poor overall survival. Increased FEZF1-AS1 expression promoted gastric cancer cell proliferation in vitro. Additionally, FEZF1-AS1 was upregulated in chemo-resistant GC tissues. The regulatory effect of FEZF1-AS1 on multi-drug resistance (MDR) in GC cells and the underlying mechanism was investigated. It was found that increased FEZF1-AS1 expression promoted chemo-resistance of GC cells. Molecular interactions were determined by RNA immunoprecipitation (RIP) and the results showed that FEZF1-AS1 regulated chemo-resistance of GC cells through modulating autophagy by directly targeting ATG5. The proliferation and autophagy of GC cells promoted by overexpression of LncFEZF1-AS1 was suppressed when ATG5 was knocked down. Moreover, knockdown of FEZF1-AS1 inhibited tumor growth and increased 5-FU sensitivity in GC cells in vivo. Taken together, this study revealed that the FEZF1-AS1/ATG5 axis regulates MDR of GC cells via modulating autophagy.

Development of a novel berberine-mediated mitochondria-targeting nano-platform for drug-resistant cancer therapy

2016 ◽  
Vol 4 (42) ◽  
pp. 6856-6864 ◽  
Author(s):  
Jue Tuo ◽  
Yanqi Xie ◽  
Jia Song ◽  
Yizhen Chen ◽  
Qin Guo ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Cancer Therapy ◽  
Tumor Growth ◽  
Tumor Cells ◽  
Multi Drug Resistance ◽  
Drug Resistant ◽  
Inhibit Tumor Growth ◽  
Mitochondria Targeting

A novel berberine-mediated mitochondria-targeting nano-platform was constructed to inhibit tumor growth and bypass the multi-drug resistance problem by targeting doxorubicin to mitochondria of tumor cells.

scholarly journals Bioinformatic analysis reveals GSG2 as a potential target for breast cancer therapy

2019 ◽  
Vol 14 (1) ◽  
pp. 688-698
Author(s):  
Zheng Ye ◽  
Zhaoyu Zhang ◽  
Lijiao Fang ◽  
Daiquan Tian ◽  
Xin Liu
Keyword(s):  
Breast Cancer ◽  
Cancer Therapy ◽  
Mrna Expression ◽  
Cancer Progression ◽  
Copy Number ◽  
Bioinformatic Analysis ◽  
Copy Number Variations ◽  
Breast Cancer Therapy ◽  
Normal Tissues ◽  
Cancer Tissues

AbstractObjectiveTo explore the potential role of GSG2 in breast cancer progression.MethodsThe mRNA expression, DNA copy number and clinical data used in this study were obtained from the TCGA data portal. The copy number variations (CNVs) thresholds were determined according to the set of discrete copy number calls provided by Genomic Identification of Significant Targets in Cancer (GISTIC).ResultsThe mRNA expression level of GSG2 in 112 breast cancer tissues was much higher than that in adjacent normal tissues. GSG2 was significantly upregulated in stage II compared with stage I, and there was no differential expression of GSG2 between tumors with or without metastasis. Heterozygous deletion occupied 57.1% of CNVs for GSG2 gene in breast cancer samples. Patients with higher GSG2 expression tended to suffer from poorer prognosis.ConclusionOur profiling analysis indicated the overexpression of GSG2 might play an important role in breast cancer development, suggesting that GSG2 could be a new target for breast cancer treatment, making GSG2 inhibitors becoming potential drugs for breast cancer therapy.

scholarly journals Mechanistic Insights Delineating the Role of Cholesterol in Epithelial Mesenchymal Transition and Drug Resistance in Cancer

2021 ◽  
Vol 9 ◽  
Author(s):  
Naaziyah Abdulla ◽  
C. Theresa Vincent ◽  
Mandeep Kaur
Keyword(s):  
Drug Resistance ◽  
Cancer Progression ◽  
Molecular Mechanisms ◽  
Epithelial Mesenchymal Transition ◽  
Cholesterol Metabolism ◽  
Cholesterol Content ◽  
Multi Drug Resistance ◽  
Mesenchymal Transition ◽  
Proposed Model

Despite the significant advancements made in targeted anti-cancer therapy, drug resistance constitutes a multifaceted phenomenon leading to therapy failure and ultimately mortality. Emerging experimental evidence highlight a role of cholesterol metabolism in facilitating drug resistance in cancer. This review aims to describe the role of cholesterol in facilitating multi-drug resistance in cancer. We focus on specific signaling pathways that contribute to drug resistance and the link between these pathways and cholesterol. Additionally, we briefly discuss the molecular mechanisms related to the epithelial-mesenchymal transition (EMT), and the documented link between EMT, metastasis and drug resistance. We illustrate this by specifically focusing on hypoxia and the role it plays in influencing cellular cholesterol content following EMT induction. Finally, we provide a proposed model delineating the crucial role of cholesterol in EMT and discuss whether targeting cholesterol could serve as a novel means of combatting drug resistance in cancer progression and metastasis.

Targeted Drug Delivery in Cancer Therapy

2005 ◽  
Vol 4 (4) ◽  
pp. 363-374 ◽  
Author(s):  
Jaspreet K. Vasir ◽  
Vinod Labhasetwar
Keyword(s):  
Drug Delivery ◽  
Drug Resistance ◽  
Cancer Therapy ◽  
Success Rate ◽  
Cancer Patients ◽  
Targeted Drug Delivery ◽  
Tumor Tissue ◽  
Tumor Biology ◽  
Multi Drug Resistance ◽  
Targeted Drug

Chemotherapy has been the main modality of treatment for cancer patients; however, its success rate remains low, primarily due to limited accessibility of drugs to the tumor tissue, their intolerable toxicity, development of multi-drug resistance, and the dynamic heterogeneous biology of the growing tumors. Better understanding of tumor biology in recent years and new targeted drug delivery approaches that are being explored using different nanosystems and bioconjugates provide optimism in developing successful cancer therapy. This article reviews the possibilities and challenges for targeted drug delivery in cancer therapy.

scholarly journals Identification of multi-drug resistance gene (MDR1) in equine ileum

2006 ◽  
Vol 36 (1) ◽  
pp. 298-300
Author(s):  
Cláudio Corrêa Natalini ◽  
Renata Lehn Linardi
Keyword(s):  
Drug Resistance ◽  
Mdr1 Gene ◽  
Multi Drug Resistance ◽  
Drug Elimination ◽  
Glycoprotein P ◽  
Future Studies ◽  
Normal Tissues ◽  
P Glycoprotein ◽  
The Central Nervous System ◽  
The Impact

P-glycoprotein (P-gp) is a membrane transporter encoded in the Multi-drug Resistance (MDR1) gene expressed in several normal tissues and over expressed in tumor cells. P-gp was already identified in different species but not yet in equine. MDR1 gene and P-gp are able to interfere with bioavailability and disposition of several drugs, altering pharmacokinetic and pharmacodinamic of drugs. The presence of the MDR1 and P-gp in the central nervous system blocks the entry of certain drugs in this tissue and reduces drug absorption and enhances drug elimination when P-gp and MDR1 are presented in the gastrointestinal tract. This study showed that the MDR1 gene is present in equine ileum. Future studies on the impact of the P-glycoprotein encoded gene MDR1 on drugs pharmacologic effects in horses are granted.

Drug induced self-assembly of triblock copolymers into polymersomes for the synergistic dual-drug delivery of platinum drugs and paclitaxel

2017 ◽  
Vol 8 (40) ◽  
pp. 6289-6299 ◽  
Author(s):  
Manuela Callari ◽  
Sandy Wong ◽  
Hongxu Lu ◽  
Janice Aldrich-Wright ◽  
Paul de Souza ◽  
...  
Keyword(s):  
Drug Delivery ◽  
Drug Resistance ◽  
Cancer Therapy ◽  
Self Assembly ◽  
Triblock Copolymers ◽  
Drug Carriers ◽  
Multi Drug Resistance ◽  
Platinum Drugs ◽  
Drug Induced ◽  
Dual Drug

Co-delivery of two drugs in one nanoparticle is increasingly used to overcome, for example, multi-drug resistance in cancer therapy and therefore suitable drug carriers need to be developed.

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