scholarly journals Adiponectin, Obesity, and Cancer: Clash of the Bigwigs in Health and Disease

2019 ◽  
Vol 20 (10) ◽  
pp. 2519 ◽  
Author(s):  
Sheetal Parida ◽  
Sumit Siddharth ◽  
Dipali Sharma
Keyword(s):  
Cancer Progression ◽  
Protective Role ◽  
The Body ◽  
Biological Functions ◽  
Anti Cancer ◽  
Guardian Angel ◽  
Health And Disease ◽  
Obesity And Cancer ◽  
Multiple Signaling

Adiponectin is one of the most important adipocytokines secreted by adipocytes and is called a “guardian angel adipocytokine” owing to its unique biological functions. Adiponectin inversely correlates with body fat mass and visceral adiposity. Identified independently by four different research groups, adiponectin has multiple names; Acrp30, apM1, GBP28, and AdipoQ. Adiponectin mediates its biological functions via three known receptors, AdipoR1, AdipoR2, and T-cadherin, which are distributed throughout the body. Biological functions of adiponectin are multifold ranging from anti-diabetic, anti-atherogenic, anti-inflammatory to anti-cancer. Lower adiponectin levels have been associated with metabolic syndrome, type 2 diabetes, insulin resistance, cardiovascular diseases, and hypertension. A plethora of experimental evidence supports the role of obesity and increased adiposity in multiple cancers including breast, liver, pancreatic, prostrate, ovarian, and colorectal cancers. Obesity mediates its effect on cancer progression via dysregulation of adipocytokines including increased production of oncogenic adipokine leptin along with decreased production of adiponectin. Multiple studies have shown the protective role of adiponectin in obesity-associated diseases and cancer. Adiponectin modulates multiple signaling pathways to exert its physiological and protective functions. Many studies over the years have shown the beneficial effect of adiponectin in cancer regression and put forth various innovative ways to increase adiponectin levels.

Cancer Fighting SiRNA-RRM2 Loaded Nanorobots

2020 ◽  
Vol 8 (2) ◽  
pp. 79-90
Author(s):  
Arjun Sharma ◽  
Pravir Kumar ◽  
Rashmi K. Ambasta
Keyword(s):  
Cancer Therapy ◽  
Dna Synthesis ◽  
Cancer Progression ◽  
Sirna Delivery ◽  
Predictive Marker ◽  
The Body ◽  
Tumor Site ◽  
Target Delivery ◽  
Target Effect

Background: Silencing of several genes is critical for cancer therapy. These genes may be apoptotic gene, cell proliferation gene, DNA synthesis gene, etc. The two subunits of Ribonucleotide Reductase (RR), RRM1 and RRM2, are critical for DNA synthesis. Hence, targeting the blockage of DNA synthesis at tumor site can be a smart mode of cancer therapy. Specific targeting of blockage of RRM2 is done effectively by SiRNA. The drawbacks of siRNA delivery in the body include the poor uptake by all kinds of cells, questionable stability under physiological condition, non-target effect and ability to trigger the immune response. These obstacles may be overcome by target delivery of siRNA at the tumor site. This review presents a holistic overview regarding the role of RRM2 in controlling cancer progression. The nanoparticles are more effective due to specific characteristics like cell membrane penetration capacity, less toxicity, etc. RRM2 have been found to be elevated in different types of cancer and identified as the prognostic and predictive marker of the disease. Reductase RRM1 and RRM2 regulate the protein and gene expression of E2F, which is critical for protein expression and progression of cell cycle and cancer. The knockdown of RRM2 leads to apoptosis via Bcl2 in cancer. Both Bcl2 and E2F are critical in the progression of cancer, hence a gene that can affect both in regulating DNA replication is essential for cancer therapy. Aim: The aim of the review is to identify the related gene whose silencing may inhibit cancer progression. Conclusion: In this review, we illuminate the critical link between RRM-E2F, RRM-Bcl2, RRM-HDAC for the therapy of cancer. Altogether, this review presents an overview of all types of SiRNA targeted for cancer therapy with special emphasis on RRM2 for controlling the tumor progression.

Role of protein S-Glutathionylation in cancer progression and development of resistance to anti-cancer drugs

2021 ◽  
Vol 704 ◽  
pp. 108890
Author(s):  
Debojyoti Pal ◽  
Archita Rai ◽  
Rahul Checker ◽  
R.S. Patwardhan ◽  
Babita Singh ◽  
...  
Keyword(s):  
Cancer Progression ◽  
Protein S ◽  
Cancer Drugs ◽  
Development Of Resistance ◽  
Anti Cancer

scholarly journals The role of m6A modification in the biological functions and diseases

2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Xiulin Jiang ◽  
Baiyang Liu ◽  
Zhi Nie ◽  
Lincan Duan ◽  
Qiuxia Xiong ◽  
...  
Keyword(s):  
Cancer Progression ◽  
Molecular Mechanisms ◽  
Target Genes ◽  
Rna Modification ◽  
Biological Functions ◽  
Rna Methylation ◽  
Downstream Target ◽  
Different Types ◽  
M6a Rna Methylation

AbstractN6-methyladenosine (m6A) is the most prevalent, abundant and conserved internal cotranscriptional modification in eukaryotic RNAs, especially within higher eukaryotic cells. m6A modification is modified by the m6A methyltransferases, or writers, such as METTL3/14/16, RBM15/15B, ZC3H3, VIRMA, CBLL1, WTAP, and KIAA1429, and, removed by the demethylases, or erasers, including FTO and ALKBH5. It is recognized by m6A-binding proteins YTHDF1/2/3, YTHDC1/2 IGF2BP1/2/3 and HNRNPA2B1, also known as “readers”. Recent studies have shown that m6A RNA modification plays essential role in both physiological and pathological conditions, especially in the initiation and progression of different types of human cancers. In this review, we discuss how m6A RNA methylation influences both the physiological and pathological progressions of hematopoietic, central nervous and reproductive systems. We will mainly focus on recent progress in identifying the biological functions and the underlying molecular mechanisms of m6A RNA methylation, its regulators and downstream target genes, during cancer progression in above systems. We propose that m6A RNA methylation process offer potential targets for cancer therapy in the future.

scholarly journals A Dual Role of Heme Oxygenase-1 in Cancer Cells

2018 ◽  
Vol 20 (1) ◽  
pp. 39 ◽  
Author(s):  
Shih-Kai Chiang ◽  
Shuen-Ei Chen ◽  
Ling-Chu Chang
Keyword(s):  
Cell Death ◽  
Heme Oxygenase ◽  
Cancer Progression ◽  
Critical Role ◽  
Causative Factor ◽  
Protective Role ◽  
Dark Side ◽  
Heme Oxygenase 1 ◽  
Cellular Iron

Heme oxygenase (HO)-1 is known to metabolize heme into biliverdin/bilirubin, carbon monoxide, and ferrous iron, and it has been suggested to demonstrate cytoprotective effects against various stress-related conditions. HO-1 is commonly regarded as a survival molecule, exerting an important role in cancer progression and its inhibition is considered beneficial in a number of cancers. However, increasing studies have shown a dark side of HO-1, in which HO-1 acts as a critical mediator in ferroptosis induction and plays a causative factor for the progression of several diseases. Ferroptosis is a newly identified iron- and lipid peroxidation-dependent cell death. The critical role of HO-1 in heme metabolism makes it an important candidate to mediate protective or detrimental effects via ferroptosis induction. This review summarizes the current understanding on the regulatory mechanisms of HO-1 in ferroptosis. The amount of cellular iron and reactive oxygen species (ROS) is the determinative momentum for the role of HO-1, in which excessive cellular iron and ROS tend to enforce HO-1 from a protective role to a perpetrator. Despite the dark side that is related to cell death, there is a prospective application of HO-1 to mediate ferroptosis for cancer therapy as a chemotherapeutic strategy against tumors.

scholarly journals Changes in Adult Rats’ Testis structure Induced by Hypothyroidism and Alleviating Role of L-Carnitine

2019 ◽  
Vol 1 (4) ◽  
pp. 13-28
Author(s):  
Abdelmonem Awad Hegazy ◽  
Manal Mohammad Morsy ◽  
Rania Said Moawad ◽  
Gehad Mohammad Elsayed
Keyword(s):  
Fatty Acids ◽  
Semen Analysis ◽  
Protective Role ◽  
The Body ◽  
Albino Rats ◽  
Adult Rats ◽  
Fatty Acids Metabolism ◽  
Group 3 ◽  
Group 2

Background Hypothyroidism is a metabolic disorder affecting the functions of many tissues in the body including the testis. Testis is rich in the polyunsaturated fatty acids content and lacks strong intrinsic antioxidant system making it prone to such oxidative stress. L-carnitine (LC) regulates long chain fatty acids metabolism; and is considered a valuable antioxidant factor. Aim It was to evaluate the effect of hypothyroidism induced by propylthiouracil (PTU) on rats’ testes and the possible protective role of LC. Methods Forty-eight adult male albino rats were used in this work. The animals were divided into three groups with sixteen animals in each. Group 1 (Control): Animals were kept without medications. Group 2 (PTU-treated): was subjected to administration of PTU; while group 3 (PTU and LC) received both PTU and LC. By the end of the experiment “30 days”, blood samples were taken for hormonal assay; then animals were anaesthetized and sacrificed. Specimens were homogenized for biochemical analysis; epididymal content of each rat was obtained immediately for semen analysis. Testes’ specimens were harvested, prepared and examined by light microscope examination. Results Induced hypothyroidism was noticed to cause histopathological, morphometric and biochemical changes in rat’s testes. LC protected the testicular specimens against such changes; it also improved the seminal quality and quantity as well as testicular structure and biochemistry. Conclusion Hypothyroidism could result in hazards to the structure of testis. Fortunately co-administration of LC might reduce such hazards.

Pathogenesis as a problem of functional incompetence and imbalance in the population of T-lymphocytes

2021 ◽  
pp. 109-119
Author(s):  
Н.М. Геворкян ◽  
Н.В. Тишевская
Keyword(s):  
T Lymphocytes ◽  
Personalized Medicine ◽  
The Body ◽  
Lymphoid Cells ◽  
Human Diseases ◽  
Regulatory Role ◽  
Total Rna ◽  
Physiological Processes ◽  
Health And Disease

Цель обзора - анализ клеточной основы патогенеза различных заболеваний в свете регуляторной роли Т-лимфоцитов. Рассматривается роль поликлонального многообразия популяции Т-лимфоцитов, особых свойств этих клеток-представителей гомеостатической системы организма в физиологических процессах в норме и при патологии. Указаны перспективы терапевтического и профилактического воздействий, связанные с использованием суммарных РНК нормальных лимфоидных клеток аллогенной и ксеногенной природы. Указана также возможность создания с помощью лимфоцитарных суммарных РНК адекватных моделей заболеваний человека на пути к развитию персонифицированной медицины. This review provides an analysis of the cellular basis of the pathogenesis of various diseases in the light of the regulatory role of T-lymphocytes. The role of the polyclonal diversity of the population of T-lymphocytes, the special properties of these cells-representatives of the homeostatic system of the body, in physiological processes in health and disease is considered. Prospects for therapeutic and prophylactic effects associated with the use of total RNA of normal lymphoid cells of allogeneic and xenogenic origin are indicated. The possibility of creating, using lymphocytic total RNA, adequate models of human diseases for the development of personalized medicine is also indicated.

Crosstalk between cancer and haemostasis

2012 ◽  
Vol 32 (02) ◽  
pp. 95-104 ◽  
Author(s):  
C. Bokemeyer ◽  
F. Langer
Keyword(s):  
Cancer Progression ◽  
Tumour Progression ◽  
Modern Concept ◽  
Anti Cancer ◽  
Haematogenous Metastasis ◽  
Triangular Network ◽  
Cell Dissemination ◽  
Patient Subgroups ◽  
Tumour Cell Dissemination

SummaryCancer is characterized by bidirectional interrelations between tumour progression, coagulation activation, and inflammation. Tissue factor (TF), the principal initiator of the coagulation protease cascade, is centrally positioned in this complex triangular network due to its pleiotropic effects in haemostasis, angiogenesis, and haematogenous metastasis. While formation of macroscopic thrombi is the correlate of cancer-associated venous thromboembolism (VTE), a major healthcare burden in clinical haematology and oncology, microvascular thrombosis appears to be critically important to blood-borne tumour cell dissemination. In this regard, expression of TF in malignant tissues as well as shedding of TFbearing microparticles into the circulation are thought to be regulated by defined genetic events relevant to pathological cancer progression, thus directly linking Trousseau’s syndrome to molecular tumourigenesis.Because pharmacological inhibition of the TF pathway in selective tumour types and patient subgroups would be in line with the modern concept of individualized, targeted anti-cancer therapy, this review will focus on the role of TF in tumour biology and cancer-associated VTE.

scholarly journals Mitochondrial Iron in Human Health and Disease

2019 ◽  
Vol 81 (1) ◽  
pp. 453-482 ◽  
Author(s):  
Diane M. Ward ◽  
Suzanne M. Cloonan
Keyword(s):  
Human Health ◽  
Mammalian Cells ◽  
Molecular Mechanisms ◽  
Innate Immune ◽  
Biological Functions ◽  
Mitochondrial Homeostasis ◽  
Innate Immune Signaling ◽  
Mitochondrial Iron ◽  
Health And Disease

Mitochondria are an iconic distinguishing feature of eukaryotic cells. Mitochondria encompass an active organellar network that fuses, divides, and directs a myriad of vital biological functions, including energy metabolism, cell death regulation, and innate immune signaling in different tissues. Another crucial and often underappreciated function of these dynamic organelles is their central role in the metabolism of the most abundant and biologically versatile transition metals in mammalian cells, iron. In recent years, cellular and animal models of mitochondrial iron dysfunction have provided vital information in identifying new proteins that have elucidated the pathways involved in mitochondrial homeostasis and iron metabolism. Specific signatures of mitochondrial iron dysregulation that are associated with disease pathogenesis and/or progression are becoming increasingly important. Understanding the molecular mechanisms regulating mitochondrial iron pathways will help better define the role of this important metal in mitochondrial function and in human health and disease.

scholarly journals Selenium and vascular health

2011 ◽  
Vol 84 (2) ◽  
pp. 239-248 ◽  
Author(s):  
Alan A. Sneddon
Keyword(s):  
Oxidative Damage ◽  
Protective Role ◽  
The Body ◽  
Vascular Health ◽  
Vascular Cells ◽  
Optimal Health ◽  
Oxidative Challenge ◽  
Se Status

Selenium (Se) is an important dietary micronutrient required for sustaining optimal health. Se is incorporated into proteins, many of which are antioxidants that protect the body against oxidative damage. As oxidative damage may contribute to the development of chronic diseases including cardiovascular disease (CVD), Se has been proposed to provide a protective role against this disease. Studies in vitro and in animals continue to provide increasing insight into the role of Se in promoting vascular health and ameliorating CVD. Se within vascular cells limits the adhesion together of such cells, an important early step in the development of vascular disease. Organic forms of Se may also afford vascular cells greater protection against oxidative challenge compared to inorganic forms. Nevertheless, current studies in humans investigating the relationship between Se and CVD have so far proved equivocal; larger randomized trials with different Se exposures in populations spanning the broad physiological Se status are needed to determine the criteria whereby Se may influence CVD outcome within different populations. Further studies are also needed to explore the effects of different Se species and the role of different selenoprotein genotypes in modifying Se status and their resultant impact on cardiovascular function.

The role of microvesicles in cancer progression and drug resistance

2013 ◽  
Vol 41 (1) ◽  
pp. 293-298 ◽  
Author(s):  
Samireh Jorfi ◽  
Jameel M. Inal
Keyword(s):  
Drug Resistance ◽  
Multidrug Resistance ◽  
Cancer Progression ◽  
Chemotherapeutic Agents ◽  
Malignant Cells ◽  
Intercellular Transport ◽  
Wide Range ◽  
Anti Cancer ◽  
Mdr Multidrug Resistance

Microvesicles are shed constitutively, or upon activation, from both normal and malignant cells. The process is dependent on an increase in cytosolic Ca2+, which activates different enzymes, resulting in depolymerization of the actin cytoskeleton and release of the vesicles. Drug resistance can be defined as the ability of cancer cells to survive exposure to a wide range of anti-cancer drugs, and anti-tumour chemotherapeutic treatments are often impaired by innate or acquired MDR (multidrug resistance). Microvesicles released upon chemotherapeutic agents prevent the drugs from reaching their targets and also mediate intercellular transport of MDR proteins.

Sign in / Sign up

Export Citation Format

Share Document