migration capacity
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Biology ◽  
2022 ◽  
Vol 11 (1) ◽  
pp. 145
Author(s):  
Cristina Almeida ◽  
Ana Luísa Teixeira ◽  
Francisca Dias ◽  
Vera Machado ◽  
Mariana Morais ◽  
...  

Colorectal cancer (CRC) is the third most common cancer in the world and represents the third most deadly tumor worldwide. About 15–25% of patients present metastasis in the moment of diagnosis, the liver being the most common site of metastization. Therefore, the development of new therapeutic agents is needed, to improve the patients’ prognosis. Amino acids transporters, LAT1 and ASCT2, are described as upregulated in CRC, being associated with a poor prognosis. Extracellular vesicles have emerged as key players in cell-to-cell communication due to their ability to transfer biomolecules between cells, with a phenotypic impact on the recipient cells. Thus, this study analyzes the presence of LAT1 and ASCT2 mRNAs in CRC-EVs and evaluates their role in phenotype modulation in a panel of four recipient cell lines (HCA-7, HEPG-2, SK-HEP-1, HKC-8). We found that HCT 116-EVs carry LAT1, ASCT2 and other oncogenic mRNAs being taken up by recipient cells. Moreover, the HCT 116-EVs’ internalization was associated with the increase of LAT1 mRNA in SK-HEP-1 cells. We also observed that HCT 116-EVs induce a higher cell migration capacity and proliferation of SK-HEP-1 and HKC-8 cells. The present study supports the LAT1-EVs’ mRNA involvement in cell phenotype modulation, conferring advantages in cell migration and proliferation.


2022 ◽  
Vol 12 (1) ◽  
Author(s):  
Guillermo Albericio ◽  
Susana Aguilar ◽  
Jose Luis Torán ◽  
Rosa Yañez ◽  
Juan Antonio López ◽  
...  

AbstractClinical trials evaluating cardiac progenitor cells (CPC) demonstrated feasibility and safety, but no clear functional benefits. Therefore a deeper understanding of CPC biology is warranted to inform strategies capable to enhance their therapeutic potential. Here we have defined, using a label-free proteomic approach, the differential cytoplasmic and nuclear compartments of human CPC (hCPC). Global analysis of cytoplasmic repertoire in hCPC suggested an important hypoxia response capacity and active collagen metabolism. In addition, comparative analysis of the nuclear protein compartment identified a significant regulation of a small number of proteins in hCPC versus human mesenchymal stem cells (hMSC). Two proteins significantly upregulated in the hCPC nuclear compartment, IL1A and IMP3, showed also a parallel increase in mRNA expression in hCPC versus hMSC, and were studied further. IL1A, subjected to an important post-transcriptional regulation, was demonstrated to act as a dual-function cytokine with a plausible role in apoptosis regulation. The knockdown of the mRNA binding protein (IMP3) did not negatively impact hCPC viability, but reduced their proliferation and migration capacity. Analysis of a panel of putative candidate genes identified HMGA2 and PTPRF as IMP3 targets in hCPC. Therefore, they are potentially involved in hCPC proliferation/migration regulation.


2021 ◽  
Author(s):  
Brais Bea-Mascato ◽  
Elena Neira-Goyanes ◽  
Antia Iglesias-Rodriguez ◽  
Diana Valverde

Background: ALMS1 is a ubiquitous gene associated with Alström syndrome (ALMS). The main symptoms of ALMS affect multiple organs and tissues, generating at last, multi-organic fibrosis in the lungs, kidneys and liver. TGF-β is one of the main pathways implicated in fibrosis, controlling the cell cycle, apoptosis, cell migration, and epithelial-mesenchymal transition (EMT). Nevertheless, the role of ALMS1 gene in fibrosis generation and other implicated processes such as cell migration or epithelial-mesenchymal transition via the TGF-β pathway has not been elucidated yet. Methods: Initially, we evaluated how depletion of ALMS1 affects different processes like apoptosis, cell cycle and mitochondrial activity. Then, we performed proteomic profiling with TGF-β stimuli in HeLa ALMS1 -/- cells and validated the results by examining different EMT biomarkers using qPCR. The expression of these EMT biomarkers was validated in hTERT-BJ-5ta. Finally, we also evaluated the SMAD3 phosphorylation in BJ-5ta model and its cell migration capacity. Results: Depletion of ALMS1 generated apoptosis resistance to thapsigargin (THAP) and C2-Ceramide (C2-C), and G2/M cell cycle arrest in HeLa cells. For mitochondrial activity, results did not show significant differences between ALMS1 +/+ and ALMS1 -/-. Proteomic results showed inhibition of downstream pathways regulated by TGF-β. The protein-coding genes (PCG) were associated with processes like focal adhesion or cell-substrate adherens junction. EMT biomarkers VIM, DSP, and SNAI1 showed an opposite pattern to what would be expected when activating the EMT. Finally, inhibition of SNAI1 was consistent in BJ-5ta model, where a reduced activation of SMAD3 and a decrease in migratory capacity were also observed. Conclusion: ALMS1 has a role in controlling the cell cycle and the apoptosis processes. Moreover, the depletion of ALMS1 inhibits the signal transduction through the TGF-β/SMAD3/SNAI1, which could be affecting the cell migration capacity and EMT.


Minerals ◽  
2021 ◽  
Vol 11 (12) ◽  
pp. 1381
Author(s):  
Li Zhang ◽  
Chitiphon Chuaicham ◽  
Vellaichamy Balakumar ◽  
Bunsho Ohtani ◽  
Keiko Sasaki

The Fe(III)-doped montmorillonite (Mt)/TiO2 composites were fabricated by adding Fe(III) during or after the aging of TiO2/Ti(OH)4 sol–gel in Mt, named as xFe-Mt/(1 − x)Fe-TiO2 and Fe/Mt/TiO2, respectively. In the xFe-Mt/(1 − x)Fe-TiO2, Fe(III) cations were expected to be located in the structure of TiO2, in the Mt, and in the interface between them, while Fe(III) ions are physically adsorbed on the surfaces of the composites in the Fe/Mt/TiO2. The narrower energy bandgap (Eg) lower photo-luminescence intensity were observed for the composites compared with TiO2. Better photocatalytic performance for phenol degradation was observed in the Fe/Mt/TiO2. The 94.6% phenol degradation was due to greater charge generation and migration capacity, which was confirmed by photocurrent measurements and electrochemical impedance spectroscopy (EIS). The results of the energy-resolved distribution of electron traps (ERDT) suggested that the Fe/Mt/TiO2 possessed a larger amorphous rutile phase content in direct contact with crystal anatase than that of the xFe-Mt/(1 − x)Fe-TiO2. This component is the fraction that is mainly responsible for the photocatalytic phenol degradation by the composites. As for the xFe-Mt/(1 − x)Fe-TiO2, the active rutile phase was followed by isolated amorphous phases which had larger (Eg) and which did not act as a photocatalyst. Thus, the physically adsorbed Fe(III) enhanced light adsorption and avoided charge recombination, resulting in improved photocatalytic performance. The mechanism of the photocatalytic reaction with the Fe(III)-doped Mt/TiO2 composite was proposed.


Author(s):  
Yago Juste-Lanas ◽  
Pedro E Guerrero ◽  
Daniel Camacho-Gomez ◽  
Silvia Hervas-Raluy ◽  
J.M. García-Aznar ◽  
...  

Abstract Metastasis, a hallmark of cancer development, is also the leading reason for most cancer-related deaths. Furthermore, cancer cells are highly adaptable to microenvironments and can migrate along pre-existing channel-like tracks of anatomical structures. However, more representative three-dimensional models are required to reproduce the heterogeneity of metastatic cell migration in vivo to further understand the metastasis mechanism and develop novel therapeutic strategies against it. Here, we designed and fabricated different microfluidic-based devices that recreate confined migration and diverse environments with asymmetric hydraulic resistances. Our results show different migratory potential between metastatic and nonmetastatic cancer cells in confined environments. Moreover, although nonmetastatic cells have not been tested against barotaxis due to their low migration capacity, metastatic cells present an enhanced preference to migrate through the lowest resistance path, being sensitive to barotaxis. This device, approaching the study of metastasis capability based on confined cell migration and barotactic cell decisions, may pave the way for the implementation of such technology to determine and screen the metastatic potential of certain cancer cells.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Hoai Huong Thi Le ◽  
Chen-wei Liu ◽  
Philip Denaro ◽  
Jordan Jousma ◽  
Ning-Yi Shao ◽  
...  

Abstract Background Electronic-cigarette (e-cig) usage, particularly in the youth population, is a growing concern. It is known that e-cig causes endothelial dysfunction, which is a risk factor for the development of cardiovascular diseases; however, the mechanisms involved remain unclear. We hypothesized that long noncoding RNAs (lncRNAs) may play a role in e-cig-induced endothelial dysfunction. Methods Here, we identified lncRNAs that are dysregulated in human induced pluripotent stem cell-derived endothelial cells (iPSC-ECs) following 24 h of e-cig aerosol extract treatment via microarray analysis. We performed Gene Ontology and Kyoto Encyclopedia of Genes and Genome (KEGG) pathway analyses of the dysregulated mRNAs following e-cig exposure and constructed co-expression networks of the top 5 upregulated lncRNAs and the top 5 downregulated lncRNAs and the mRNAs that are correlated with them. Furthermore, the functional effects of knocking down lncRNA lung cancer-associated transcript 1 (LUCAT1) on EC phenotypes were determined as it was one of the significantly upregulated lncRNAs following e-cig exposure based on our profiling. Results 183 lncRNAs and 132 mRNAs were found to be upregulated, whereas 297 lncRNAs and 413 mRNAs were found to be downregulated after e-cig exposure. We also observed that e-cig caused dysregulation of endothelial metabolism resulting in increased FAO activity, higher mitochondrial membrane potential, and decreased glucose uptake and glycolysis. These results suggest that e-cig alters EC metabolism by increasing FAO to compensate for energy deficiency in ECs. Finally, the knockdown of LUCAT1 prevented e-cig-induced EC dysfunction by maintaining  vascular barrier, reducing reactive oxygen species level, and increasing migration capacity. Conclusion This study identifies an expression profile of differentially expressed lncRNAs and several potential regulators and pathways in ECs exposed to e-cig, which provide insights into the regulation of lncRNAs and mRNAs and the role of lncRNA and mRNA networks in ECs associated e-cig exposure.


2021 ◽  
Author(s):  
Chun Wang ◽  
Feng Yao

Background: Atherosclerosis (AS) induced cardiology disease is largely associated with morbidity and mortality. The dysfunction of vascular smooth muscle cells (VSMCs) is considered to contribute to the etiology of AS. However, the mechanism underlying VSMCs dysfunction remains largely unclear. Our study aimed to explore novel molecules mediating VSMCs function. Methods: Bioinformatical analysis was applied to identify the key miRNAs that was aberrantly expressed in AS mouse and potentially targeted TFPI2. The AS-like cell model was generated by treating VSMCs with ox-LDL. The expression level of miR-513a-5p and TFPI2 in VSMCs and the serum of AS patients was evaluated by RT-qPCR, and the expression level of TFPI2 and PCNA was measured by western blot. The cell viability and migration capacity of VSMCs were determined by CCK-8 and wound healing assay, respectively. The target relationship between miR-513a-5p and TFPI2 was validated by dual-luciferase assay. Results: MiR-513a-5p was highly expressed while TFPI2 presented a low expression in AS patient serum. Treatment with 100 μg/mL ox-LDL overtly facilitated the cell viability and migration of VSMCs, also promoted miR-513a-5p expression while limit the expression of TFPI2. Moreover, silencing miR-513a-5p inhibited the cell viability, migration and the expression of proliferative marker in ox-LDL treated VSMCs, while inhibition of TFPI2 enhanced that. It was further found that miR-513a-5p could target TFPI2 and silencing miR-513a-5p compromised the aggresive effect of TFPI2 inhibition on the viability and migration ox-LDL treated VSMCs. Conclusion: miR-513a-5p could contribute to the dysfunction of VSMCs in AS through targeting and inhibiting TFPI2.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Elham Barazeghi ◽  
Per Hellman ◽  
Olov Norlén ◽  
Gunnar Westin ◽  
Peter Stålberg

AbstractSmall intestinal neuroendocrine tumors (SI-NETs) are slow-growing tumors that seem genetically quite stable without highly recurrent mutations, but are epigenetically dysregulated. In contrast to the undetectable expression of the enhancer of zeste homolog 2 (EZH2) histone methyltransferase in the enterochromaffin cells of the small intestine, we found high and differential expression of EZH2 in primary SI-NETs and corresponding metastases. Silencing EZH2 in the SI-NET cell line CNDT2.5 reduced cell proliferation and induced apoptosis. Furthermore, EZH2 knockout inhibited tumor progression in a CNDT2.5 SI-NET xenograft mouse model, and treatment of SI-NET cell lines CNDT2.5 and GOT1 with the EZH2-specific inhibitor CPI-1205 decreased cell viability and promoted apoptosis. Moreover, CPI-1205 treatment reduced migration capacity of CNDT2.5 cells. The EZH2 inhibitor GSK126 also repressed proliferation of CNDT2.5 cells. Recently, metformin has received wide attention as a therapeutic option in diverse cancers. In CNDT2.5 and GOT1 cells, metformin suppressed EZH2 expression, and inhibited cell proliferation. Exposure of GOT1 three-dimensional cell spheroids to CPI-1205 or metformin arrested cell proliferation and decreased spheroid size. These novel findings support a possible role of EZH2 as a candidate oncogene in SI-NETs, and suggest that CPI-1205 and metformin should be further evaluated as therapeutic options for patients with SI-NETs.


Biomedicines ◽  
2021 ◽  
Vol 9 (11) ◽  
pp. 1727
Author(s):  
Jun-Ho Lee ◽  
So-Yeon Choi ◽  
Soo-Yeoun Park ◽  
Nam-Chul Jung ◽  
Kyung-Eun Noh ◽  
...  

Enpp2 is an enzyme that catalyzes the conversion of lysophosphatidylcholine (LPC) to lysophosphatidic acid (LPA), which exhibits a wide variety of biological functions. Here, we examined the biological effects of Enpp2 on dendritic cells (DCs), which are specialized antigen-presenting cells (APCs) characterized by their ability to migrate into secondary lymphoid organs and activate naïve T-cells. DCs were generated from bone marrow progenitors obtained from C57BL/6 mice. Enpp2 levels in DCs were regulated using small interfering (si)RNA or recombinant Enpp2. Expression of Enpp2 in LPS-stimulated mature (m)DCs was high, however, knocking down Enpp2 inhibited mDC function. In addition, the migratory capacity of mDCs increased after treatment with rmEnpp2; this phenomenon was mediated via the RhoA-mediated signaling pathway. Enpp2-treated mDCs showed a markedly increased capacity to migrate to lymph nodes in vivo. These findings strongly suggest that Enpp2 is necessary for mDC migration capacity, thereby increasing our understanding of DC biology. We postulate that regulating Enpp2 improves DC migration to lymph nodes, thus improving the effectiveness of cancer vaccines based on DC.


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