scholarly journals Understanding the complexity of Epimorphic Regeneration in zebrafish: A Transcriptomic and Proteomic approach.

2021 ◽  
Author(s):  
Sarena Banu ◽  
Namami Gaur ◽  
Sowmy Nair ◽  
Tanuja Ravikrishnan ◽  
Shahida Khan ◽  
...  
Keyword(s):  
Differential Expression Analysis ◽  
Cell Movement ◽  
Molecular Transport ◽  
Caudal Fin ◽  
Tissue Samples ◽  
Fin Regeneration ◽  
Epimorphic Regeneration ◽  
Proteomic Approach ◽  
Generation Sequencing

Genomic and Proteomic changes play a crucial role in perpetuating regeneration of complex tissues through differentiation and growth. The complex Epimorphic regeneration of zebrafish caudal fin tissue is hasty and absolute. This study was executed to understand the role of various genes/proteins involved in the regeneration of zebrafish caudal fin tissue through differential expression analysis. High throughput transcriptomics analysis involving Next Generation Sequencing approach and iTRAQ based quantitative proteomics analyses were performed on the regenerating tissue samples for various regenerating time points. Based on our study 1408 genes and 661 proteins were found differentially regulated in the regenerating caudal fin tissue for having at least 1-log fold change in their expression at 12hpa, 1, 2, 3 and 7dpa stages against control non-regenerating tissue. Interleukin, SLC, PRMT, HOX, neurotransmitter and several novel genes were found to be associated with regeneration for its differential regulation during the mechanism. Based on the network and pathway analysis the differentially regulated genes and proteins were found allied with activation of cell proliferation, cell viability, cell survival & cell movement and inactivation of organismal death, morbidity, necrosis, death of embryo & cell death. Network pathways such as Cancer & development disorder, Cell signaling molecular transport, organismal injury & abnormalities and Cellular development, growth & proliferation were found most significantly associated with the zebrafish caudal fin regeneration mechanism. This study has mapped a detailed insight of the genes/proteins expression associated with the epimorphic regeneration more profoundly.

scholarly journals Functional Role of Annexins in Zebrafish Caudal Fin Regeneration – A Gene Knockdown Approach in Regenerating Tissue

2018 ◽  
Author(s):  
Mir Quoseena ◽  
Sowmya Vuppaladadium ◽  
Shahid Hussain ◽  
Swarna Bharathi ◽  
Mohammed M Idris
Keyword(s):  
Functional Role ◽  
Target Genes ◽  
Human Beings ◽  
Caudal Fin ◽  
Fin Regeneration ◽  
Epimorphic Regeneration ◽  
Knock Down ◽  
Regeneration Mechanism ◽  
Almost All

AbstractRegeneration is an adaptive phenomenon with wide biological implications spread heterogeneously in almost all the organism including human beings. The ability of regeneration varies from species to species for its impediment. Epimorphic regeneration of zebrafish caudal fin tissue is most widely studied regeneration mechanism for its discrete and rapid regenerative capability. Several genes/proteins were found to be associated with zebrafish caudal fin tissue regeneration. Here, we have evaluated the functional role ofAnnexin 2aand2bgenes in adult zebrafish caudal fin tissue undergoing regeneration using a novel CRSISPR-Cas9 gene knock down approach. Knock down of both the genes individually elicited in decelerated regeneration and down regulation of target genes and its partner genes/proteins such as ANXA1a, ANXA5b and ANXA13. This study validates a novel gene targeting approach and the possible role of annexin in regeneration mechanism.

Role of Hox genes in zebrafish caudal fin regeneration

2006 ◽  
Vol 25 ◽  
pp. S25-S25
Author(s):  
M SARRASJR ◽  
R THUMMEL ◽  
A GODMAN
Keyword(s):  
Hox Genes ◽  
Caudal Fin ◽  
Fin Regeneration

Role of annexin gene and its regulation during zebrafish caudal fin regeneration

2016 ◽  
Vol 24 (3) ◽  
pp. 551-559 ◽  
Author(s):  
Sandeep Saxena ◽  
Sruthi Purushothaman ◽  
Vuppalapaty Meghah ◽  
Bhawna Bhatti ◽  
Akhila Poruri ◽  
...  
Keyword(s):  
Caudal Fin ◽  
Fin Regeneration ◽  
Annexin Gene

scholarly journals Inhibition of BMP and FGF signaling prior to wound epithelium formation leads to an aberrant regenerative response in teleost fish Poecilia latipinna

2021 ◽  
Author(s):  
Isha Ranadive ◽  
Sonam Patel ◽  
Siddharth Pai ◽  
Kashmira Khaire ◽  
Suresh Balakrishnan
Keyword(s):  
Cell Death ◽  
Teleost Fish ◽  
The Other ◽  
Fgf Signaling ◽  
Caudal Fin ◽  
Fin Regeneration ◽  
Blastema Formation ◽  
Messenger Molecules ◽  
Wound Epithelium

The BMP and FGF pathways play a pivotal role in the successful regeneration of caudal fin of teleost fish. Individual inhibition of these pathways led to impaired caudal fin regeneration until the pharmacologic inhibitor of FGF (SU5402) and BMP (LDN193189) were metabolized off. Therefore, in the current study both these pathways were inhibited collectively wherein inhibition of BMP and FGF during the wound epithelium formation led to stalling of the process by bringing down the established levels of shh and runx2. In members of the treatment group, it was observed that, each blastema grows crouched rather than linear and the regrown lepidotrichia therefore remain tilted down. Amongst the other irregularities observed, the transition from epithelial to mesenchymal cells was found hindered due to down-regulation of snail and twist, brought about by BMP and FGF inhibition. Compromised expression of Snail and twist deranged the normal levels of cadherins causing disruption in the transition of cells. Lastly, blocking BMP and FGF delayed blastema formation and proliferation due to diminished levels of fgf2, fgf8, fgf10 and bmp6, while casp3 and casp9 levels remained heightened causing accelerated cell death. This study not only highlights the axial role of BMP and FGF pathways in regeneration but also accentuates the collaboration amongst the two. This ingenious coordination of signalling further reinforces the involvement of relaying messenger molecules between these crucial pathways.

scholarly journals Functional role of annexins in zebrafish caudal fin regeneration – A gene knockdown approach in regenerating tissue

Biochimie ◽  
2020 ◽  
Vol 175 ◽  
pp. 125-131 ◽  
Author(s):  
Mir Quoseena ◽  
Sowmya Vuppaladadium ◽  
Shahid Hussain ◽  
Sarena Banu ◽  
Swarna Bharathi ◽  
...  
Keyword(s):  
Functional Role ◽  
Gene Knockdown ◽  
Caudal Fin ◽  
Fin Regeneration

scholarly journals The Role of Liquid Biopsy in Hepatocellular Carcinoma Prognostication

Cancers ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 659 ◽  
Author(s):  
Ismail Labgaa ◽  
Augusto Villanueva ◽  
Olivier Dormond ◽  
Nicolas Demartines ◽  
Emmanuel Melloul
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liquid Biopsy ◽  
Biological Fluids ◽  
Tissue Samples ◽  
Genomic Complexity ◽  
Minimally Invasive Access ◽  
Next Generation Sequencing Ngs ◽  
Generation Sequencing ◽  
Related Mortality

Showing a steadily increasing cancer-related mortality, the epidemiological evolution of hepatocellular carcinoma (HCC) is concerning. Numerous strategies have attempted to prognosticate HCC but their performance is modest; this is partially due to the heterogeneous biology of this cancer. Current clinical guidelines endorse classifications and scores that use clinical variables, such as the Barcelona Clinic Liver Cancer (BCLC) classification. These algorithms are unlikely to fully recapitulate the genomic complexity of HCC. Integrating molecular readouts on a patient-basis, following a precision-medicine perspective, might be an option to refine prognostic systems. The limited access to HCC tissue samples is an important limitation to these approaches but it could be partially circumvented by using liquid biopsy. This concept consists of the molecular analysis of products derived from a solid tumor and released into biological fluids, mostly into the bloodstream. It offers an easy and minimally-invasive access to DNA, RNA, extracellular vesicles and cells that can be analyzed with next-generation sequencing (NGS) technologies. This review aims to investigate the potential contributions of liquid biopsy in HCC prognostication. The results identified prognostic values for each of the components of liquid biopsy, suggesting that this technology may help refine HCC prognostication.

scholarly journals Alterations in esophageal microRNAs expression in primary esophageal achalasia by next-generation sequencing

2020 ◽  
Author(s):  
Mahin Gholipour ◽  
Javad Mikaeli ◽  
Seyed Javad Mowla ◽  
Mohammad Reza Bakhtiarizadeh ◽  
Marie Saghaeian Jazi ◽  
...  
Keyword(s):  
Next Generation Sequencing ◽  
Mirna Expression ◽  
Target Genes ◽  
Esophageal Achalasia ◽  
P Value ◽  
Growth Factor Signaling ◽  
Next Generation ◽  
Tissue Samples ◽  
Generation Sequencing

Abstract Background The molecular knowledge of primary esophageal achalasia is essential for the early diagnosis and treatment of this neurodegenerative motility disorder. So it is substantial to find the main microRNAs (miRNAs), which are related to mechanisms of achalasia. Methods This study aimed to determine some patterns of deregulated miRNAs in achalasia. This case-control study was performed on 52 achalasia patients and 50 non-achalasia controls. The miRNA expression profiling was conducted on esophageal tissue samples from achalasia and non-achalasia patients, via next-generation sequencing (NGS). Differential expression of miRNAs was analyzed by edgeR software. The selected dysregulated miRNAs were additionally confirmed using RT-qPCR. Potential target genes of the down-regulated and up-regulated miRNAs were also predicted to understand the putative role of the miRNAs in achalasia. Results We identified 15 miRNAs that were significantly altered in the achalasia tissues compared to controls. Among these miRNAs, three; miR-133a-5p, miR-143-3p and miR-6507-5p were up-regulated. Also we found six miRNAs; miR-215-5p, miR-216a-5p, miR-216b-5p, miR-217, miR-7641 and miR-194-5p were down-regulated significantly. The predicted targets for the dysregulated miRNAs showed significant disease-associated pathways like neuron cell apoptosis, neuromuscular balance, neuron growth factor signaling and immune response regulation. Gene expression analysis confirmed significant downregulation of hsa-miR-217 (p-value =0.004) in LES of achalasia patients with significant enrichment in myelination process ontology. This study provides the first integrated miRNA expression profile using NGS in achalasia. Our findings introduced 15 candidate microRNAs as achalasia associated non-coding RNAs genes showing confirmed downregulation of the hsa-miR-217 in Achalasia disease. Conclusions Our results may serve as a basis for more future functional studies to discover the role of candidate miRNAs in the etiology of achalasia and their application in diagnosis and probably treatment.

Current Study of RhoA and Associated Signaling Pathways in Gastric Cancer

2020 ◽  
Vol 15 (7) ◽  
pp. 607-613 ◽  
Author(s):  
Haiping Liu ◽  
Yiqian Liu ◽  
Xiaochuan Zhang ◽  
Xiaodong Wang
Keyword(s):  
Gastric Cancer ◽  
Survival Rate ◽  
Signaling Pathways ◽  
Tumor Cells ◽  
Actin Polymerization ◽  
Cell Transformation ◽  
Cell Movement ◽  
Invasion And Metastasis ◽  
Common Cancer

Gastric cancer (GC) is the fourth-most common cancer in the world, with an estimated 1.034 million new cases in 2015, and the third-highest cause of cancer deaths, estimated at 785,558, in 2014. Early diagnosis and treatment greatly affect the survival rate in patients with GC: the 5‐year survival rate of early GC reaches 90%‐95%, while the mortality rate significantly increases if GC develops to the late stage. Recently, studies for the role of RhoA in the diseases have become a hot topic, especially in the development of tumors. A study found that RhoA can regulate actin polymerization, cell adhesion, motor-myosin, cell transformation, and the ability to participate in the activities of cell movement, proliferation, migration, which are closely related to the invasion and metastasis of tumor cells. However, the specific role of RhoA in tumor cells remains to be studied. Therefore, our current study aimed to briefly review the role of RhoA in GC, especially for its associated signaling pathways involved in the GC progression.

A Novel Method for Microsatellite Instability Detection by Liquid Biopsy Based on Next- Generation Sequencing

2020 ◽  
Vol 15 ◽  
Author(s):  
Zheng Jiang ◽  
Hui Liu ◽  
Siwen Zhang ◽  
Jia Liu ◽  
Weitao Wang ◽  
...  
Keyword(s):  
Next Generation Sequencing ◽  
Microsatellite Instability ◽  
Liquid Biopsy ◽  
Tumor Tissue ◽  
High Sensitivity ◽  
Next Generation ◽  
Tissue Samples ◽  
Next Generation Sequencing Technology ◽  
Medication Selection ◽  
Generation Sequencing

Background: Microsatellite instability (MSI) is a prognostic biomarker used to guide medication selection in multiple cancers, such as colorectal cancer. Traditional PCR with capillary electrophoresis and next-generation sequencing using paired tumor tissue and leukocyte samples are the main approaches for MSI detection due to their high sensitivity and specificity. Currently, patient tissue samples are obtained through puncture or surgery, which causes injury and risk of concurrent disease, further illustrating the need for MSI detection by liquid biopsy. Methods: We propose an analytic method using paired plasma/leukocyte samples and MSI detection using next-generation sequencing technology. Based on the theoretical progress of oncogenesis, we hypothesized that the microsatellite site length in plasma equals the combination of the distribution of tumor tissue and leukocytes. Thus, we defined a window-judgement method to identify whether biomarkers were stable. Results: Compared to traditional PCR as the standard, we evaluated three methods in 20 samples (MSI-H:3/MSS:17): peak shifting method using tissue vs. leukocytes, peak shifting method using plasma vs. leukocytes, and our method using plasma vs. leukocytes. Compared to traditional PCR, we observed a sensitivity of 100%, 0%, and 100%, and a specificity of 100.00%, 94.12%, and 88.24%, respectively. Conclusion: Our method has the advantage of possibly detecting MSI in a liquid biopsy and provides a novel direction for future studies to increase the specificity of the method.

scholarly journals Possible Role of IRS-4 in the Origin of Multifocal Hepatocellular Carcinoma

Cancers ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 2560
Author(s):  
Luis G. Guijarro ◽  
Patricia Sanmartin-Salinas ◽  
Eva Pérez-Cuevas ◽  
M. Val Toledo-Lobo ◽  
Jorge Monserrat ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liver Cancer ◽  
Hepg2 Cells ◽  
Cellular Polarity ◽  
Ki 67 ◽  
Tissue Samples ◽  
Vitro Analysis ◽  
Tumoral Cells

New evidence suggests that insulin receptor substrate 4 (IRS-4) may play an important role in the promotion of tumoral growth. In this investigation, we have evaluated the role of IRS-4 in a pilot study performed on patients with liver cancer. We used immunohistochemistry to examine IRS-4 expression in biopsies of tumoral tissue from a cohort of 31 patient suffering of hepatocellular carcinoma (HCC). We simultaneously analyzed the expression of the cancer biomarkers PCNA, Ki-67, and pH3 in the same tissue samples. The in vitro analysis was conducted by studying the behavior of HepG2 cells following IRS-4 overexpression/silencing. IRS-4 was expressed mainly in the nuclei of tumoral cells from HCC patients. In contrast, in healthy cells involved in portal triads, canaliculi, and parenchymal tissue, IRS-4 was observed in the cytosol and the membrane. Nuclear IRS-4 in the tumoral region was found in 69.9 ± 3.2%, whereas in the surrounding healthy hepatocytes, nuclear IRS-4 was rarely observed. The percentage of tumoral cells that exhibited nuclear PCNA and Ki-67 were 52.1 ± 7%, 6.1 ± 1.1% and 1.3 ± 0.2%, respectively. Furthermore, we observed a significant positive linear correlation between nuclear IRS-4 and PCNA (r = 0.989; p < 0.001). However, when we correlated the nuclear expression of IRS-4 and Ki-67, we observed a significant positive curvilinear correlation (r = 0.758; p < 0.010). This allowed us to define two populations, (IRS-4 + Ki-67 ≤ 69%) and (IRS-4 + Ki-67 > 70%). The population with lower levels of IRS-4 and Ki-67 had a higher risk of suffering from multifocal liver cancer (OR = 16.66; CI = 1.68–164.8 (95%); p < 0.05). Immunoblot analyses showed that IRS-4 in normal human liver biopsies was lower than in HepG2, Huh7, and Chang cells. Treatment of HepG2 with IGF-1 and EGF induced IRS-4 translocation to the nucleus. Regulation of IRS-4 levels via HepG2 transfection experiments revealed the protein’s role in proliferation, cell migration, and cell-collagen adhesion. Nuclear IRS-4 is increased in the tumoral region of HCC. IRS-4 and Ki-67 levels are significantly correlated with the presence of multifocal HCC. Moreover, upregulation of IRS-4 in HepG2 cells induced proliferation by a β-catenin/Rb/cyclin D mechanism, whereas downregulation of IRS-4 caused a loss in cellular polarity and in its adherence to collagen as well as a gain in migratory and invasive capacities, probably via an integrin α2 and focal adhesion cascade (FAK) mechanism.

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