scholarly journals Protein Lipidation by Palmitoylation and Myristoylation in Cancer

Author(s):  
Chee Wai Fhu ◽  
Azhar Ali

Posttranslational modification of proteins with lipid moieties is known as protein lipidation. The attachment of a lipid molecule to proteins endows distinct properties, which affect their hydrophobicity, structural stability, localization, trafficking between membrane compartments, and influences its interaction with effectors. Lipids or lipid metabolites can serve as substrates for lipidation, and the availability of these lipid substrates are tightly regulated by cellular metabolism. Palmitoylation and myristoylation represent the two most common protein lipid modifications, and dysregulation of protein lipidation is strongly linked to various diseases such as metabolic syndromes and cancers. In this review, we present recent developments in our understanding on the roles of palmitoylation and myristoylation, and their significance in modulating cancer metabolism toward cancer initiation and progression.

2010 ◽  
Vol 11 (9) ◽  
pp. 1112-1120 ◽  
Author(s):  
Calli A. Davison ◽  
Zachary T. Schafer

Cancers ◽  
2021 ◽  
Vol 13 (19) ◽  
pp. 4829
Author(s):  
Nithin Sadeesh ◽  
Mauro Scaravilli ◽  
Leena Latonen

Prostate cancer is the second most frequent cancer of men worldwide. While the genetic landscapes and heterogeneity of prostate cancer are relatively well-known already, methodological developments now allow for studying basic and dynamic proteomes on a large scale and in a quantitative fashion. This aids in revealing the functional output of cancer genomes. It has become evident that not all aberrations at the genetic and transcriptional level are translated to the proteome. In addition, the proteomic level contains heterogeneity, which increases as the cancer progresses from primary prostate cancer (PCa) to metastatic and castration-resistant prostate cancer (CRPC). While multiple aspects of prostate adenocarcinoma proteomes have been studied, less is known about proteomes of neuroendocrine prostate cancer (NEPC). In this review, we summarize recent developments in prostate cancer proteomics, concentrating on the proteomic landscapes of clinical prostate cancer, cell line and mouse model proteomes interrogating prostate cancer-relevant signaling and alterations, and key prostate cancer regulator interactomes, such as those of the androgen receptor (AR). Compared to genomic and transcriptomic analyses, the view provided by proteomics brings forward changes in prostate cancer metabolism, post-transcriptional RNA regulation, and post-translational protein regulatory pathways, requiring the full attention of studies in the future.


2021 ◽  
Vol 14 ◽  
Author(s):  
Chandra Kishore

: The recent developments in epigenetics have shown a very important role of epigenetic changes in cancer initiation, development, and progression. Some of the important histone modifications shown to occur are methylation, acetylation, phosphorylation, citrullination, sumoylation, ADP ribosylation, deamination, ubiquitination, formylation, O-GlcNAcylation, propionylation, butyrylation, proline isomerization, and crotonylation but most of the studies in past had limited their studies mainly on histone methylation, acetylation, and phosphorylation. Modification of DNA strand by hypermethylation and hypomethylation regulates genomic instability and promotes cancer. Colorectal cancer involves multiple changes in epigenetic marks present on histone residues and DNA, which in collaboration with genetic changes, drives cancer progression. In this review paper, basic concepts of epigenetics relevant to cancer development are discussed followed by its significance in understanding the mechanism of colon carcinogenesis. Some of the epigenetic target based drugs are also discussed in the relevant sections to give an idea of the potential promises of epigenetics for colorectal cancer treatment.


Author(s):  
Nallanchakravarthula Srivathsa ◽  
Narayanappa Amruta ◽  
Chitteti Ramamurthy

Background: The microbes and host association emerged as a modulator in the modern era of medicine.The cancer and its associated host microbes are collectively referred to as a Cancer Microbiome. Cancer and microbiome have complex characteristics in terms of metabolic plasticity, micro environment remodelling, cellular communications and unique signatures within the host. These hallmark signs have a vital role in homeostasis and pathogenesis of host physiology.However, in the cancer the role of microbiome still needs to be explored. It is pivotal to review such hall mark signatures of microbiome and its role in cancer initiation, progression and therapy. Objective: The objective of this review is to elucidate the role of microbiome in cancer metabolism and tumour microenvi-ronment. It also focuses on importance of therapeutic opportunities and challenges in terms of manipulation of cancer mi-crobiome. Methods: The literature search is based on the notion of microbiome has role in cancer initiation, progression and therapy. Conclusion: The tumour micro environment and cancer metabolism are playing a significant in host-microbiome interactions. Microbiome can modulate the typical cancer therapies like chemo and immuno therapies in standard of care. The microbiome transplantation has been demonstrated as an effective therapy against cancer. Furthermore, the modulation of microbiome also has potential clinical outcomes in modern medicine.


2021 ◽  
Vol 11 ◽  
Author(s):  
Kasey R. Cargill ◽  
William L. Hasken ◽  
Carl M. Gay ◽  
Lauren A. Byers

Metabolic reprogramming is a hallmark of cancer initiation, progression, and relapse. From the initial observation that cancer cells preferentially ferment glucose to lactate, termed the Warburg effect, to emerging evidence indicating that metabolic heterogeneity and mitochondrial metabolism are also important for tumor growth, the complex mechanisms driving cancer metabolism remain vastly unknown. These unique shifts in metabolism must be further investigated in order to identify unique therapeutic targets for individuals afflicted by this aggressive disease. Although novel therapies have been developed to target metabolic vulnerabilities in a variety of cancer models, only limited efficacy has been achieved. In particular, lung cancer metabolism has remained relatively understudied and underutilized for the advancement of therapeutic strategies, however recent evidence suggests that lung cancers have unique metabolic preferences of their own. This review aims to provide an overview of essential metabolic mechanisms and potential therapeutic agents in order to increase evidence of targeted metabolic inhibition for the treatment of lung cancer, where novel therapeutics are desperately needed.


2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Ke Fang ◽  
Wei Huang ◽  
Yu-Meng Sun ◽  
Tian-Qi Chen ◽  
Zhan-Cheng Zeng ◽  
...  

Abstract Background Long noncoding enhancer RNAs (lnc-eRNAs) are a subset of stable eRNAs identified from annotated lncRNAs. They might act as enhancer activity-related therapeutic targets in cancer. However, the underlying mechanism of epigenetic activation and their function in cancer initiation and progression remain largely unknown. Results We identify a set of lncRNAs as lnc-eRNAs according to the epigenetic signatures of enhancers. We show that these lnc-eRNAs are broadly activated in MLL-rearranged leukemia (MLL leukemia), an aggressive leukemia caused by a chromosomal translocation, through a mechanism by which the HOXA cluster initiates enhancer activity, and the epigenetic reader BRD4 cooperates with the coregulator MLL fusion oncoprotein to induce transcriptional activation. To demonstrate the functional roles of lnc-eRNAs, two newly identified lnc-eRNAs transcribed from the SEELA eRNA cluster (SEELA), SEELA1 and SEELA2, are chosen for further studies. The results show that SEELA mediated cis-activated transcription of the nearby oncogene Serine incorporate 2 (SERINC2) by directly binding to the K31 amino acid (aa) of histone H4. Chromatin-bound SEELA strengthens the interaction between chromatin and histone modifiers to promote histone recognition and oncogene transcription. Further studies show that the SEELA-SERINC2 axis regulated aspects of cancer metabolism, such as sphingolipid synthesis, to affect leukemia progression. Conclusions This study shows that lnc-eRNAs are epigenetically activated by cancer-initiating oncoproteins and uncovers a cis-activating mechanism of oncogene transcription control based on lnc-eRNA-mediated epigenetic regulation of enhancer activity, providing insights into the critical roles of lnc-eRNAs in cancer initiation and progression.


Author(s):  
C. Colliex ◽  
P. Trebbia

The physical foundations for the use of electron energy loss spectroscopy towards analytical purposes, seem now rather well established and have been extensively discussed through recent publications. In this brief review we intend only to mention most recent developments in this field, which became available to our knowledge. We derive also some lines of discussion to define more clearly the limits of this analytical technique in materials science problems.The spectral information carried in both low ( 0<ΔE<100eV ) and high ( >100eV ) energy regions of the loss spectrum, is capable to provide quantitative results. Spectrometers have therefore been designed to work with all kinds of electron microscopes and to cover large energy ranges for the detection of inelastically scattered electrons (for instance the L-edge of molybdenum at 2500eV has been measured by van Zuylen with primary electrons of 80 kV). It is rather easy to fix a post-specimen magnetic optics on a STEM, but Crewe has recently underlined that great care should be devoted to optimize the collecting power and the energy resolution of the whole system.


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