Ion channels and transporters in cancer. 4. Remodeling of Ca2+ signaling in tumorigenesis: role of Ca2+ transport

2011 ◽  
Vol 301 (5) ◽  
pp. C969-C976 ◽  
Author(s):  
Jane M. Lee ◽  
Felicity M. Davis ◽  
Sarah J. Roberts-Thomson ◽  
Gregory R. Monteith

The Ca2+ signal has major roles in cellular processes important in tumorigenesis, including migration, invasion, proliferation, and apoptotic sensitivity. New evidence has revealed that, aside from altered expression and effects on global cytosolic free Ca2+ levels via direct transport of Ca2+, some Ca2+ pumps and channels are able to contribute to tumorigenesis via mechanisms that are independent of their ability to transport Ca2+ or effect global Ca2+ homeostasis in the cytoplasm. Here, we review some of the most recent studies that present evidence of altered Ca2+ channel or pump expression in tumorigenesis and discuss the importance and complexity of localized Ca2+ signaling in events critical for tumor formation.

2018 ◽  
Vol 19 (7) ◽  
pp. 2060 ◽  
Author(s):  
Magdalena Bachmann ◽  
Roberto Costa ◽  
Roberta Peruzzo ◽  
Elena Prosdocimi ◽  
Vanessa Checchetto ◽  
...  

In recent years, several experimental evidences have underlined a new role of ion channels in cancer development and progression. In particular, mitochondrial ion channels are arising as new oncological targets, since it has been proved that most of them show an altered expression during tumor development and the pharmacological targeting of some of them have been demonstrated to be able to modulate cancer growth and progression, both in vitro as well as in vivo in pre-clinical mouse models. In this scenario, pharmacology of mitochondrial ion channels would be in the near future a new frontier for the treatment of tumors. In this review, we discuss the new advances in the field, by focusing our attention on the improvements in new drug developments to target mitochondrial ion channels.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Qi He ◽  
Zhenyu Li

AbstractCaMK2 (calcium/calmodulin-dependent protein kinase 2), a multifunctional serine/threonine-protein kinase involved in diverse cellular processes, is vital for the transduction of the Ca2+ signaling cascade. Recently, research has highlighted the involvement of CaMK2 in cancer development. However, the specific effects of CaMK2 on cancer have not been fully elucidated. In this review, we summarize not only the altered expression of CaMK2 in a range of cancers, as evidenced by bioinformatics analysis, but also the significant role of CaMK2 in regulating cancer progression, such as proliferation and metastasis. In addition, we described the functional influence of CaMK2 on cancer stemness and resistance. Understanding the critical effects and mechanisms of CaMK2 in cancer would facilitate the development of a promising therapeutic strategy for cancer treatment.


2021 ◽  
Author(s):  
◽  
Janet Youkhana

<p>Cyclic di-guanosine-monophosphate (c-di-GMP) has been recognized as a second messenger in bacteria controlling multiple cellular processes such as biofilm formation, motility, and virulence. Proteins containing GGDEF and EAL domains are engaged in the synthesis and degradation, respectively, of cyclic di-GMP. Some bacteria contain multiple proteins with GGDEF and EAL domains. The genome of Mycobacterium tuberculosis encodes only one protein (Rv1354c) which contains a GGDEF domain. This protein also contains a tandem EAL. The function of this protein in mycobacteria has not yet been determined. In this study, the orthologue of Rv1354c was investigated in Mycobacterium smegmatis (MSMEG_2196). The expression of MSMEG_2196 in M. smegmatis was altered by constructing sense and antisense expressing strains. The effect of the altered expression of MSMEG_2196 on M. smegmatis was tested under carbon, oxygen, phosphorous, and nitrogen limited growth conditions. There was no significant effect on growth in either the antisense or sense expressing strains grown under nutrient-rich, or carbon-, or oxygen-, or phosphorous limitation conditions. However, a growth effect was observed in the antisense expressing strain when grown under nitrogen-limited conditions. In particular, at mid stationary-phase (1,800 min) the MSMEG_2196 antisense strain had an OD600 value of 0.60, compared to that of the control M. smegmatis/pMind strain (OD600 value of 1.09). These results were further confirmed by the low colony forming units measures observed in MSMEG_2196 antisense strain. Proteomic analysis was carried out on the MSMEG_2196 antisesne expressing strain grown in the nitrogen-limited condition. Proteins that were differentially expressed were identified by mass spectrometry. A number of the proteins that were down-regulated in the antisense expressing strain are important in the survival of the bacteria under nitrogen-limited conditions. This study indicates a role for MSMEG_2196 in growth or survival of mycobacteria under nitrogen-limitations.</p>


2018 ◽  
Vol 5 (2) ◽  
pp. 8-15
Author(s):  
I. F. Gareev ◽  
O. A. Beylerli

MicroRNAs are a new class of small non-coding RNAs, a length of 18–22 nucleotides that play a decisive role as posttranscriptional regulators of gene expression. Due to the large number of genes, regulated microRNAs, microRNAs are involved in many cellular processes. The study of the impairment of the expression of the target genes of microRNA, often associated with changes in important biological characteristics, provides a significant understanding of the role of microRNAs in oncogenesis. New evidence suggests that aberrant microRNA expression or dysregulation of endogenous microRNAs affects the onset and development of tumors, including adenomas of the pituitary gland. In this review, the significance of some microRNAs in the pathology of the pituitary adenoma will be assessed, as well as data on the study of microRNAs as therapeutic targets and new biomarkers.


2011 ◽  
Vol 301 (6) ◽  
pp. C1281-C1289 ◽  
Author(s):  
V'yacheslav Lehen'kyi ◽  
George Shapovalov ◽  
Roman Skryma ◽  
Natalia Prevarskaya

Ion channels contribute to virtually all basic cellular processes, including such crucial ones for maintaining tissue homeostasis as proliferation, differentiation, and apoptosis. The involvement of ion channels in regulation of programmed cell death, or apoptosis, has been known for at least three decades based on observation that classical blockers of ion channels can influence cell death rates, prolonging or shortening cell survival. Identification of the central role of these channels in regulation of cell cycle and apoptosis as well as the recent discovery that the expression of ion channels is not limited solely to the plasma membrane, but may also include membranes of internal compartments, has led researchers to appreciate the pivotal role of ion channels plays in development of cancer. This review focuses on the aspects of programmed cell death influenced by various ion channels and how dysfunctions and misregulations of these channels may affect the development and progression of different cancers.


2019 ◽  
Vol 22 (3) ◽  
pp. 283-293 ◽  
Author(s):  
H. Rafieemehr ◽  
A. Samimi ◽  
M. Maleki Behzad ◽  
M. Ghanavat ◽  
S. Shahrabi

2021 ◽  
Vol 11 (6) ◽  
pp. 500
Author(s):  
Margherita Ferrante ◽  
Antonio Cristaldi ◽  
Gea Oliveri Conti

The daily environmental exposure of humans to plasticizers may adversely affect human health, representing a global issue. The altered expression of microRNAs (miRNAs) plays an important pathogenic role in exposure to plasticizers. This systematic review summarizes recent findings showing the modified expression of miRNAs in cancer due to exposure to plasticizers. Following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) methodology, we performed a systematic review of the literature published in the past 10 years, focusing on the relationship between plasticizer exposure and the expression of miRNAs related to cancer. Starting with 535 records, 17 articles were included. The results support the hypothesis that exposure to plasticizers causes changes in or the deregulation of a number of oncogenic miRNAs and show that the interaction of plasticizers with several redundant miRNAs, such as let-7f, let-7g, miR-125b, miR-134, miR-146a, miR-22, miR-192, miR-222, miR-26a, miR-26b, miR-27b, miR-296, miR-324, miR-335, miR-122, miR-23b, miR-200, miR-29a, and miR-21, might induce deep alterations. These genotoxic and oncogenic responses can eventually lead to abnormal cell signaling pathways and metabolic changes that participate in many overlapping cellular processes, and the evaluation of miRNA-level changes can be a useful target for the toxicological assessment of environmental pollutants, including plastic additives and plasticizers.


Author(s):  
Margherita Ferrante ◽  
Antonio Cristaldi ◽  
Gea Oliveri Conti

The environmental exposure of human in the daily and occupational activities to plasticizers may adversely affect human health, and thus represents a global issue. The altered expression of MicroRNAs (miRNAs) exerts an important pathogenic role linked also to the exposure to plasticizers. This systematic review summarizes the recent findings showing modified ex-pression of miRNAs in cancer due to plasticizers exposures. Following Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) methodology, we performed a systematic review of the past ten years, focusing on the relationship between plasticizer exposures and expression of miRNAs cancer. Starting by 535 records, 17 articles were included. Results support the hypothesis that exposure to plasticizers cause changes or deregulation of a number of oncogenic miRNAs and showed that plasticizers interaction with several redundant miRNAs, such as let-7f, let-7g, miR-125b, miR-134, miR-146a, miR-22; miR-192, miR-222, miR-26a, miR-26b, miR-27b, miR-296, miR-324, miR-335, miR-122, miR-23b, miR-200, miR-29a and miR-21, might induce deep alterations. These genotoxic and oncogenic responses can eventually lead to abnormal cell signaling pathways and metabolisms that participate in many overlapped cellular processes, and miRNA level changes can be a useful tool for the toxicological assessment of environmental pollutants, including plastic additives and plasticizers


2021 ◽  
Author(s):  
Yanyan Li ◽  
Jungang Zhao ◽  
Renpin Chen ◽  
Shengwei Chen ◽  
Yilun Xu ◽  
...  

Abstract Background: Lipid metabolism has a profound impact on gastric cancer (GC) progression and is a newly targetable vulnerability for cancer therapy. Given the importance of lipids in cancer cellular processes, in this study we employed lipidomic clinical and transcriptomic data of GC to connect the variations of lipid metabolism changes.Method: We constructed a clinical nomogram based on the lipid factors and other clinical items. Then by using multi-omics techniques, we established a lipid-related gene signature for individualized prognosis prediction in patients with GC. Moreover, a total of 1357 GC cases were then applied to evaluate the robustness of this model. WGCNA was used to identify co-expression modules and enriched genes associated with GC lipid metabolism. The role of key genes ACLY in GC was further investigated.Results: The prognostic value of the lipidomic signature was analyzed using Cox regression model, and clinical nomogram was established. Among them, we observed overexpression of ACLY significantly increased the levels of intracellular free fatty acid and triglyceride, and activate AKT/mTOR pathway to promote cancer development.Conclusions: In conclusion, our findings delineated a GC clinical and lipidomic signature and revealed that GC exhibited a reprogramming of lipid metabolism in association with an altered expression of lipid metabolism-associated genes. Among them, ACLY significantly promoted GC lipid metabolism and increased cancer cell proliferation, suggesting that this pathway can be targetable as a metabolic vulnerability in future GC therapy.


2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Yonggang Wang ◽  
Xiao Miao ◽  
Yucheng Liu ◽  
Fengsheng Li ◽  
Quan Liu ◽  
...  

Cardiovascular disease (CVD) remains a leading cause of mortality worldwide despite advances in its prevention and management. A comprehensive understanding of factors which contribute to CVD is required in order to develop more effective treatment options. Dysregulation of epigenetic posttranscriptional modifications of histones in chromatin is thought to be associated with the pathology of many disease models, including CVD. Histone acetyltransferases (HATs) and deacetylases (HDACs) are regulators of histone lysine acetylation. Recent studies have implicated a fundamental role of reversible protein acetylation in the regulation of CVDs such as hypertension, pulmonary hypertension, diabetic cardiomyopathy, coronary artery disease, arrhythmia, and heart failure. This reversible acetylation is governed by enzymes that HATs add or HDACs remove acetyl groups respectively. New evidence has revealed that histone acetylation regulators blunt cardiovascular and related disease states in certain cellular processes including myocyte hypertrophy, apoptosis, fibrosis, oxidative stress, and inflammation. The accumulating evidence of the detrimental role of histone acetylation in cardiac disease combined with the cardioprotective role of histone acetylation regulators suggests that the use of histone acetylation regulators may serve as a novel approach to treating the millions of patients afflicted by cardiac diseases worldwide.


Sign in / Sign up

Export Citation Format

Share Document