scholarly journals Glutathione S-Transferases in Cancer

Antioxidants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 701
Author(s):  
Rahul Raj Singh ◽  
Katie M. Reindl
Keyword(s):  
Cell Proliferation ◽  
Drug Resistance ◽  
Clinical Trials ◽  
Antioxidant Enzymes ◽  
Cancer Treatment ◽  
Cell Survival ◽  
Structural Similarity ◽  
Cancer Development ◽  
Pharmacological Studies ◽  
Glutathione S Transferases

In humans, the glutathione S-transferases (GST) protein family is composed of seven members that present remarkable structural similarity and some degree of overlapping functionalities. GST proteins are crucial antioxidant enzymes that regulate stress-induced signaling pathways. Interestingly, overactive GST proteins are a frequent feature of many human cancers. Recent evidence has revealed that the biology of most GST proteins is complex and multifaceted and that these proteins actively participate in tumorigenic processes such as cell survival, cell proliferation, and drug resistance. Structural and pharmacological studies have identified various GST inhibitors, and these molecules have progressed to clinical trials for the treatment of cancer and other diseases. In this review, we discuss recent findings in GST protein biology and their roles in cancer development, their contribution in chemoresistance, and the development of GST inhibitors for cancer treatment.

Mechanism of long-chain non-coding RNA hypoxia-inducible factor 1α-antisense RNA 1 regulating chemotherapy resistance of retinoblastoma by inhibiting hypoxia-inducible factor-α expression

2021 ◽  
Vol 11 (11) ◽  
pp. 1874-1880
Author(s):  
Cao Gu ◽  
Qing Li ◽  
Shaofei Zhao ◽  
Yu Gao ◽  
Peirong Lu
Keyword(s):  
Cell Proliferation ◽  
Drug Resistance ◽  
Cell Survival ◽  
Treatment Effectiveness ◽  
Hypoxia Inducible Factor ◽  
Chemotherapy Resistance ◽  
Non Coding Rna ◽  
Reduce Cell Proliferation ◽  
Factor Α ◽  
Infants And Young Children

Retinoblastoma (Rb) mostly occurs in infants and young children with weak resistance. Surgical treatment causes great damage to children’s appearance, so adjuvant chemotherapy is needed to reduce the damage. But chemotherapeutic resistance affects treatment effectiveness and may even lead to the death of the child. Exploring the specific mechanism of drug resistance in Rb children is helpful to improve the therapeutic effect. It was found that the relative expression in Rb cell Y79, SO-Rb50, and HXO-Rb44 was greatly higher than that in normal hum an retinal cells. After transfection of SI-HIF1A-AS1 into Rb cells, the expression of lncRNA HIF1A-AS1 was decreased greatly, and the level of HIF-1α was down-regulated. Suppress lncRNA HIF1A-AS1 expression can reduce cell proliferation and improve apoptosis. Based on the overexpression of HIF-1α, the cell proliferation ability was restored partially, and the apoptosis ability was reduced greatly. When cells were cultured with vincristine, we found that suppress lncRNA HIF1A-AS1 expression can decrease cell survival, and overexpression of HIF-1α improved cell survival. The above results confirmed that inhibition of lncRNA HIF1AAS1 expression could reduce drug resistance of Y97 cells, while overexpression of HIF-1α can antagonize the drug resistance of low expression lncRNA HIF1A-AS1 against Rb cells. Therefore, this study suggests that lncRNA HIF1A-AS1 may regulate Rb cells’ resistance to vincristine by regulating HIF-1α expression.

scholarly journals The Complex Network between MYC Oncogene and microRNAs in Gastric Cancer: An Overview

2020 ◽  
Vol 21 (5) ◽  
pp. 1782 ◽  
Author(s):  
Ana Carolina Anauate ◽  
Mariana Ferreira Leal ◽  
Danielle Queiroz Calcagno ◽  
Carolina Oliveira Gigek ◽  
Bruno Takao Real Karia ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Drug Resistance ◽  
Complex Network ◽  
Causes Of Death ◽  
Noncoding Rnas ◽  
Protein Translation ◽  
Cancer Development ◽  
Cancer Treatments ◽  
Myc Oncogene

Despite the advancements in cancer treatments, gastric cancer is still one of the leading causes of death worldwide. In this context, it is of great interest to discover new and more effective ways of treating this disease. Accumulated evidences have demonstrated the amplification of 8q24.21 region in gastric tumors. Furthermore, this is the region where the widely known MYC oncogene and different microRNAs are located. MYC deregulation is key in tumorigenesis in various types of tissues, once it is associated with cell proliferation, survival, and drug resistance. microRNAs are a class of noncoding RNAs that negatively regulate the protein translation, and which deregulation is related with gastric cancer development. However, little is understood about the interactions between microRNAs and MYC. Here, we overview the MYC role and its relationship with the microRNAs network in gastric cancer aiming to identify potential targets useful to be used in clinic, not only as biomarkers, but also as molecules for development of promising therapies.

scholarly journals Targeting chemokines for acute lymphoblastic leukemia therapy

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Zixi Hong ◽  
Zimeng Wei ◽  
Tian Xie ◽  
Lin Fu ◽  
Jiaxing Sun ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Drug Resistance ◽  
Clinical Trials ◽  
Acute Lymphoblastic Leukemia ◽  
Hematological Malignancy ◽  
Lymphoblastic Leukemia ◽  
Leukemia Cell ◽  
Clonal Expansion ◽  
Disease Relapse ◽  
Preclinical Trials

AbstractAcute lymphoblastic leukemia (ALL) is a hematological malignancy characterized by the malignant clonal expansion of lymphoid hematopoietic precursors. It is regulated by various signaling molecules such as cytokines and adhesion molecules in its microenvironment. Chemokines are chemotactic cytokines that regulate migration, positioning and interactions of cells. Many chemokine axes such as CXCL12/CXCR4 and CCL25/CCR9 have been proved to play important roles in leukemia microenvironment and further affect ALL outcomes. In this review, we summarize the chemokines that are involved in ALL progression and elaborate on their roles and mechanisms in leukemia cell proliferation, infiltration, drug resistance and disease relapse. We also discuss the potential of targeting chemokine axes for ALL treatments, since many related inhibitors have shown promising efficacy in preclinical trials, and some of them have entered clinical trials.

scholarly journals The Role of CDK5 in Tumours and Tumour Microenvironments

Cancers ◽  
2020 ◽  
Vol 13 (1) ◽  
pp. 101
Author(s):  
Phuong Anh Do ◽  
Chang Hoon Lee
Keyword(s):  
Immune Response ◽  
Cell Proliferation ◽  
Protein Kinase ◽  
Cancer Treatment ◽  
Tumour Progression ◽  
Cancer Development ◽  
Cyclin Dependent Kinase ◽  
Neuronal Function ◽  
Cyclin Dependent Kinase 5

Cyclin-dependent kinase 5 (CDK5), which belongs to the protein kinase family, regulates neuronal function but is also associated with cancer development and has been proposed as a target for cancer treatment. Indeed, CDK5 has roles in cell proliferation, apoptosis, angiogenesis, inflammation, and immune response. Aberrant CDK5 activation triggers tumour progression in numerous types of cancer. In this review, we summarise the role of CDK5 in cancer and neurons and CDK5 inhibitors. We expect that our review helps researchers to develop CDK5 inhibitors as treatments for refractory cancer.

scholarly journals Epitranscriptomic Approach: To Improve the Efficacy of ICB Therapy by Co-targeting Intracellular Checkpoint CISH

2021 ◽  
Author(s):  
Sunil Kumar ◽  
Parth Sarthi ◽  
Indra Mani ◽  
Muhammad Umer Ashraf ◽  
Myeong-Ho Kang ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Clinical Trials ◽  
Monoclonal Antibodies ◽  
Cancer Treatment ◽  
Immune Surveillance ◽  
Cellular Immunotherapy ◽  
High Dose ◽  
Functional Importance ◽  
Surveillance Mechanism ◽  
Shed Light

Cellular immunotherapy has recently emerged as a fourth pillar in cancer treatment co-joining surgery, chemotherapy and radiotherapy. Where, the discovery of immune checkpoint blockage or inhibition (ICB/ICI), anti-PD-1/PD-L1 and anti-CTLA4-based, therapy has revolutionized the class of cancer treatment at a different level. However, still some cancer patient escape this immune surveillance mechanism and become resistant to ICB-therapy. Therefore, a more advanced or an alternative treatment is required instantly. Despite the functional importance of epitranscriptomics in diverse clinico-biological practices, its role in improving the efficacy of ICB therapeutics has been limited. Consequently, our study encapsulates the evidences, as a possible strategy, to improve the efficacy of ICB-therapy by co-targeting molecular checkpoints especially N6A-modification machineries which could be reformed into RNA modifying drugs (RMD). Here, we have explained the mechanism of individual RNA-modifiers (editor/writer, eraser/remover and effector/reader) in overcoming the issues associated with high-dose antibody toxicities and drug-resistance. Moreover, we have shed light on the importance of suppressor of cytokine signalling (SOCS/CISH) and microRNAs in improving the efficacy of ICB-therapy, with brief insight on the current monoclonal antibodies undergoing clinical trials or already approved against several solid tumor and metastatic cancers. We anticipate our investigation will encourage researchers and clinicians to further strengthen the efficacy of ICB-therapeutics by considering the importance of epitranscriptomics as a personalized medicine.

Oncogenic LncRNA CASC9 in Cancer Progression

2020 ◽  
Vol 26 ◽  
Author(s):  
Yuying Qi ◽  
Chaoying Song ◽  
Jiali Zhang ◽  
Chong Guo ◽  
Chengfu Yuan
Keyword(s):  
Cell Proliferation ◽  
Drug Resistance ◽  
Cell Growth ◽  
Cancer Cells ◽  
Therapeutic Potential ◽  
Squamous Metaplasia ◽  
Neoplastic Transformation ◽  
Over Expression ◽  
Human Cancers ◽  
Current Review

Background: Long non-coding RNA (LncRNAs), with the length over 200 nucleotides, originate from intergenic, antisense, or promoter-proximal regions, is a large family of RNAs that lack coding capacity. Emerging evidences illustrated that LncRNAs played significant roles in a variety of cellular functions and biological processes in profuse human diseases, especially in cancers. Cancer susceptibility candidate 9 (CASC9), as a member of the LncRNAs group, was firstly found its oncogenic function in esophageal cancer. In following recent studies, a growing amount of human malignancies are verified to be correlated with CASC9, most of which are derived from the squamous epithelium tissue. This present review attempts to highlight the latest insights into the expression, functional roles, and molecular mechanisms of CASC9 in different human malignancies. Methods: In this review, the latest findings related to the pathophysiological processes of CASC9 in human cancers were summarized and analyzed, the associated studies were collected in systematically retrieval of PubMed used lncRNA and CASA9 as keywords. Results: CASC9 expression is identified to be aberrantly elevated in a variety of malignancies. The over-expression of CASC9 has been suggested to accelerate cell proliferation, migration, cell growth and drug resistance of cancer cells, while depress cell apoptosis, revealing its role as an oncogene. Moreover, the current review demonstrated CASC9 closely relates to neoplastic transformation of squamous epithelial cells and squamous metaplasia in non-squamous epithelial tissues. Finally, we discuss the limitations and tremendous diagnostic/therapeutic potential of CASC9 in various human cancers. Results: CASC9 expression is identified to be aberrantly elevated in a variety of malignancies. The over-expression of CASC9 has been suggested to accelerate cell proliferation, migration, cell growth and drug resistance of cancer cells, while depress cell apoptosis, revealing its role as an oncogene. Moreover, the current review demonstrated CASC9 closely relates to neoplastic transformation of squamous epithelial cells and squamous metaplasia in non-squamous epithelial tissues. Finally, we discuss the limitations and tremendous diagnostic/therapeutic potential of CASC9 in various human cancers. Conclusion: Long non-coding RNACASC9 likely served as useful disease biomarkers or therapy targets that could effectively apply in treatment of different kinds of cancers.

A Critical Review of Second-generation anti-EGFR Monoclonal Antibodies in Metastatic Colorectal Cancer

2020 ◽  
Vol 21 ◽  
Author(s):  
Daniel Sur ◽  
Andrei Havasi ◽  
Alecsandra Gorzo ◽  
Claudia Burz
Keyword(s):  
Colorectal Cancer ◽  
Drug Resistance ◽  
Clinical Trials ◽  
Monoclonal Antibodies ◽  
Metastatic Colorectal Cancer ◽  
Second Generation ◽  
Current Data ◽  
Braf Mutations ◽  
Durable Response ◽  
Ongoing Research

Background: Anti-EGFR monoclonal antibodies (mAbs) have become a relevant solution for the treatment of patients with metastatic colorectal cancer. Current anti-EGFR monoclonal antibodies face a series of problems, including resistance and non-durable response, and RAS and BRAF mutations serve as exclusion criteria for treatment with anti-EGFR mAbs. Advances in molecular tumor profiling and information on subsequent pathways responsible for disease progression and drug resistance helped develop a new generation of anti-EGFR mAbs. These second-generation mAbs have been developed to overcome existing resistance mechanisms and to limit common side effects. For the moment, existing literature suggests that these novel anti-EGFR mAbs are far from finding their way to clinical practice soon. Objective: In this review, we summarize and evaluate current data regarding ongoing research and completed clinical trials for different second-generation anti-EGFR monoclonal antibodies. Conclusion: Anti-EGFR mAbs exhibit efficacy in advanced colorectal cancer, but second-generation mAbs failed to prove their benefit in the treatment of metastatic colorectal cancer. Understanding the biological basis of primary and acquired drug resistance could allow scientists to design better clinical trials and develop improved second-generation mAbs.

scholarly journals Non-Steroidal Anti-Inflammatory Drugs in Colorectal Cancer Chemoprevention

Cancers ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 594
Author(s):  
Jadwiga Maniewska ◽  
Dagmara Jeżewska
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Clinical Trials ◽  
Cancer Chemoprevention ◽  
Tumor Cell Proliferation ◽  
Double Blind ◽  
New Approach ◽  
Randomized Controlled ◽  
Inflammatory Drugs ◽  
Chemopreventive Effect

Since colorectal cancer is one of the world’s most common cancers, studies on its prevention and early diagnosis are an emerging area of clinical oncology these days. For this study, a review of randomized controlled, double-blind clinical trials of selected NSAIDs (aspirin, sulindac and celecoxib) in chemoprevention of colorectal cancer was conducted. The main molecular anticancer activity of NSAIDs is thought to be a suppression of prostaglandin E2 synthesis via cyclooxygenase-2 inhibition, which causes a decrease in tumor cell proliferation, angiogenesis, and increases apoptosis. The lower incidence of colorectal cancer in the NSAID patients suggests the long-lasting chemopreventive effect of drugs studied. This new approach to therapy of colorectal cancer may transform the disease from a terminal to a chronic one that can be taken under control.

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