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Search results for: CD29

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#39490753   2024/10/26 To Up

MiRNA29a-3p Negatively Regulates ISL1-Integrin β1 Axis to Suppress Gastric Cancer Progression.

Insulin gene enhancer protein 1 (ISL1) belongs to the LIM homeodomain transcription factor family, which is closely related to the development of several cancers. We previously found that abnormally high ISL1 expression is involved in gastric cancer (GC) metastasis. However, the specific role of ISL1 and its regulatory mechanisms in GC metastasis warrant elucidation. In this study, we found that ISL1 is highly expressed in GC tissues and positively correlated with GC development, promoting cell migration and invasion in vivo and in vitro. Moreover, miRNA29a-3p can target ISL1 and thus inhibit GC cell migration. Furthermore, ISL1 upregulates ITGB1 by binding to its enhancer; nevertheless, ISL1-ITGB1 axis expression can be regulated using miRNA29a-3p. In GC cell nuclei, ISL1 and annexin A2 (ANXA2) form a transcriptional activator complex at the ITGB1 enhancer, thus promoting ITGB1 expression. In GC cell cytoplasm, the ISL1-ANXA2 complex synergistically activates matrix metalloproteinases, thus promoting cell migration. In conclusion, ISL1 is a potential therapeutic target for GC.
Ziwei She, Haosheng Dong, Yang Li, Ping Chen, Chunyan Zhou, Weiping Wang, Zhuqing Jia, Qiong Shi

1498 related Products with: MiRNA29a-3p Negatively Regulates ISL1-Integrin β1 Axis to Suppress Gastric Cancer Progression.



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#39486657   2024/10/30 To Up

The IPR inhibitor desmethylxestospongin B reduces tumor cell migration, invasion and metastasis by impairing lysosome acidification and β1-integrin recycling.

Cancer is the second leading cause of death worldwide. >90 % of cancer-related deaths are due to metastasis, a process that depends on the ability of cancer cells to leave the primary tumor, migrate, and colonize different tissues. Inositol 1,4,5-trisphosphate receptor (IPR)-mediated Ca signaling plays an essential role in maintaining the homeostasis of cancer cells and the sustained proliferation. Desmethylxestospongin B (dmXeB) is a specific inhibitor of the IPR that selectively arrests cell proliferation and promotes cancer cell death at high concentrations. However, whether migration, invasion and metastasis can be affected by this drug is unknown. Here, by using the highly metastatic triple negative breast cancer (TNBC) cell line MDA-MB-231, we demonstrate that a prolonged inhibition of IPR-mediated Ca signals with dmXeB significantly reduces cell migration and invasion in vitro and metastasis in vivo. We found that this phenomenon was independent of the bioenergetic control of IPR over the mitochondria and AMPK activation. Furthermore, employing a tandem LC3-GFP-mcherry assay, we found that prolonged inhibition of IPR with dmXeB leads to diminished autophagic flux. This reduction can be attributed to impaired lysosomal acidification, as evidenced by assessments using DQ-BSA and pHrodo. Since cell migration requires appropriate assembly and disassembly of focal adhesions, along with the internalization and recycling of integrins via autophagy, we explored the dependency of integrin recycling from autophagosomes, finding that IPR inhibition with dmXeB impaired the recycling of β1-integrins, which accumulated within autophagosomes. Our findings reveal an unexpected effect of IPR inhibition with dmXeB in cancer cells that could represent a novel therapeutic strategy for the treatment of cancer metastasis.
Galdo Bustos, Ulises Ahumada-Castro, Eduardo Silva-Pavez, Hernán Huerta, Andrea Puebla, Camila Quezada, Pablo Morgado-Cáceres, César Casanova-Canelo, Natalia Smith-Cortinez, Maša Podunavac, Cesar Oyarce, Alvaro Lladser, Paula Farias, Alenka Lovy, Jordi Molgó, Vicente A Torres, Armen Zakarian, J César Cárdenas

2404 related Products with: The IPR inhibitor desmethylxestospongin B reduces tumor cell migration, invasion and metastasis by impairing lysosome acidification and β1-integrin recycling.

5 G100 mg25 mg96T1000 TESTS/0.65ml100ug25ml25 mg

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#39473957   // To Up

Clinical significance of upregulated Rho GTPase activating protein 12 causing resistance to tyrosine kinase inhibitors in hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) is a major health challenge with high incidence and poor survival rates in China. Systemic therapies, particularly tyrosine kinase inhibitors (TKIs), are the first-line treatment for advanced HCC, but resistance is common. The Rho GTPase family member Rho GTPase activating protein 12 (ARHGAP12), which regulates cell adhesion and invasion, is a potential therapeutic target for overcoming TKI resistance in HCC. However, no studies on the expression of ARHGAP12 in HCC and its role in resistance to TKIs have been reported.
Xiao-Wei Wang, Yu-Xing Tang, Fu-Xi Li, Jia-Le Wang, Gao-Peng Yao, Da-Tong Zeng, Yu-Lu Tang, Bang-Teng Chi, Qin-Yan Su, Lin-Qing Huang, Di-Yuan Qin, Gang Chen, Zhen-Bo Feng, Rong-Quan He

1944 related Products with: Clinical significance of upregulated Rho GTPase activating protein 12 causing resistance to tyrosine kinase inhibitors in hepatocellular carcinoma.

8 inhibitors5 inhibitors102 Pieces/Box

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#39469031   2024/10/23 To Up

Elevated MMP-9, Survivin, TGB1 and Downregulated Tissue Inhibitor of TIMP-1, Caspase-3 Activities are Independent of the Low Levels miR-183 in Endometriosis.

This study aimed to measure the correlation between miR-183 and gene expression that regulates apoptosis and adhesion mechanism that may be linked to the pathogenesis of endometriosis.
R Muharam, Anom Bowolaksono, Mila Maidarti, Ririn Rahmala Febri, Kresna Mutia, Pritta Ameilia Iffanolida, Muhammad Ikhsan, Kanadi Sumapraja, Gita Pratama, Achmad Kemal Harzif, Andon Hestiantoro, Budi Wiweko

2998 related Products with: Elevated MMP-9, Survivin, TGB1 and Downregulated Tissue Inhibitor of TIMP-1, Caspase-3 Activities are Independent of the Low Levels miR-183 in Endometriosis.

100.00 ug96T20 µl (10 mM)20 20 ul (10 mM)100 ul (2 mM)100 assays100 µl (2 mM)20 100 µl1 mg

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#39468184   2024/10/28 To Up

Modeling a biofluid-derived extracellular vesicle surface signature to differentiate pediatric idiopathic nephrotic syndrome clinical subgroups.

Idiopathic Nephrotic Syndrome (INS) is a common childhood glomerular disease requiring intense immunosuppressive drug treatments. Prediction of treatment response and the occurrence of relapses remains challenging. Biofluid-derived extracellular vesicles (EVs) may serve as novel liquid biopsies for INS classification and monitoring. Our cohort was composed of 105 INS children at different clinical time points (onset, relapse, and persistent proteinuria, remission, respectively), and 19 healthy controls. The expression of 37 surface EV surface markers was evaluated by flow cytometry in serum (n = 83) and urine (n = 74) from INS children (mean age = 10.1, 58% males) at different time points. Urine EVs (n = 7) and serum EVs (n = 11) from age-matched healthy children (mean age = 7.8, 94% males) were also analyzed. Tetraspanin expression in urine EVs was enhanced during active disease phase in respect to the remission group and positively correlates with proteinuria levels. Unsupervised clustering analysis identified an INS signature of 8 markers related to immunity and angiogenesis/adhesion processes. The CD41b, CD29, and CD105 showed the best diagnostic scores separating the INS active phase from the healthy condition. Interestingly, combining urinary and serum EV markers from the same patient improved the precision of clinical staging separation. Three urinary biomarkers (CD19, CD44, and CD8) were able to classify INS based on steroid sensitivity. Biofluid EVs offer a non-invasive tool for INS clinical subclassification and "personalized" interventions.
Giulia Cricri, Andrea Gobbini, Stefania Bruno, Linda Bellucci, Sarah Tassinari, Federico Caicci, Chiara Tamburello, Teresa Nittoli, Irene Paraboschi, Alfredo Berrettini, Renata Grifantini, Benedetta Bussolati, William Morello, Giovanni Montini, Federica Collino

2619 related Products with: Modeling a biofluid-derived extracellular vesicle surface signature to differentiate pediatric idiopathic nephrotic syndrome clinical subgroups.

1 mg1 mL 100 G200 1 mg

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#39468006   2024/10/28 To Up

Proteomic profiling reveals CEACAM6 function in driving gallbladder cancer aggressiveness through integrin receptor, PRKCD and AKT/ERK signaling.

Gallbladder cancer (GBC) presents as an aggressive malignancy with poor patient outcome. Like other epithelial cancers, the mechanisms of GBC cancer progression remain vague and efforts in finding targeted therapies fall below expectations. This study combined proteomic analysis of formalin-fixed paraffin-embedded (FFPE) GBC samples, functional and molecular characterization of potential oncogenes and identification of potential therapeutic strategies for GBC. We identified Carcinoembryonic Antigen-related Cell Adhesion Molecule 6 (CEACAM6) as one of the significantly most upregulated proteins in GBC. CEACAM6 overexpression has been observed in other cancer entities but the molecular function remains unclear. Our functional analyses in vitro and in vivo mouse models revealed that CEACAM6 supported the initial steps of cancer progression and metastasis by decreasing cell adhesion and promoting migration and invasion of GBC cells. Conversely, CEACAM6 knockdown abolished GBC aggressiveness by increasing cell adhesion while reducing cell migration, cell proliferation, and colony formation. BirA-BioID followed by mass-spectrometry revealed Integrin Beta-1 (ITGB1) and Protein Kinase C Delta (PRKCD) as direct molecular and functional partners of CEACAM6 supporting GBC cell migration. ERK and AKT signaling and their downstream target genes were regulated by CEACAM6 and thus the treatment with AKT inhibitor capivasertib or ERK inhibitor ulixertinib mitigated the CEACAM6-induced migration. These findings demonstrate that CEACAM6 is crucially involved in gallbladder cancer progression by promoting migration and inhibiting cell adhesion through ERK and AKT signaling providing specific options for treatment of CEACAM6-positive cancers.
Raisatun Nisa Sugiyanto, Carmen Metzger, Aslihan Inal, Felicia Truckenmueller, Kira Gür, Eva Eiteneuer, Thorben Huth, Angelika Fraas, Ivonne Heinze, Joanna Kirkpatrick, Carsten Sticht, Thomas Albrecht, Benjamin Goeppert, Tanja Poth, Stefan Pusch, Arianeb Mehrabi, Peter Schirmacher, Junfang Ji, Alessandro Ori, Stephanie Roessler

1095 related Products with: Proteomic profiling reveals CEACAM6 function in driving gallbladder cancer aggressiveness through integrin receptor, PRKCD and AKT/ERK signaling.

2 Pieces/Box50 ug2 Pieces/Box100ug100 μg100ug Lyophilized100ug100ug Lyophilized

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#39462866   2024/10/27 To Up

Application of mass cytometry in multiparametric characterization of precancerous cervical lesions.

Cervical cancer (CC) is the fourth most common malignant tumor in women worldwide. Detecting different biomarkers together on single cells by novel method mass cytometry could contribute to more precise screening. Liquid-based cytology (LBC) cervical samples were collected (N = 53) from women categorized as normal and precancerous lesions. Human papillomavirus was genotyped by polymerase chain reaction, while simultaneous examination of the expression of 29 proteins was done by mass cytometry (CyTOF). Differences in cluster abundances were assessed with Spearman's rank correlation as well as high dimensional data analysis (t-SNE, FlowSOM). Cytokeratin (ITGA6, Ck5, Ck10/13, Ck14, Ck7) expression patterns allowed determining the presence of different cells in the cervical epithelium. FlowSOM analysis enabled to phenotype cervical cells in five different metaclusters and find new markers that could be important in CC screening. The markers Ck18, Ck18, and CD63 (Metacluster 3) showed significantly increasing associated with severity of the precancerous lesions (Spearman rank correlation rho 0.304, p = 0.0271), while CD71, KLF4, LRIG1, E-cadherin, Nanog and p53 (Metacluster 1) decreased with severity of the precancerous lesions (Spearman rank correlation rho -0.401, p = 0.0029). Other metaclusters did not show significant correlation, but metacluster 2 (Ck17, MCM, MMP7, CD29, E-cadherin, Nanog, p53) showed higher abundance in low- and high-grade intraepithelial lesion cases. CyTOF appears feasible and should be considered when examining novel biomarkers on cervical LBC samples. This study enabled us to characterize different cells in the cervical epithelium and find markers and populations that could distinguish precancerous lesions.
Ena Pešut, Ivana Šimić, Daniela Kužilkova, Tomáš Kalina, Rajko Fureš, Ivana Erceg Ivkošić, Nina Milutin Gašperov, Ivan Sabol

2332 related Products with: Application of mass cytometry in multiparametric characterization of precancerous cervical lesions.

100ul 100ul 100ul1mg0.1ml 100ul1 kit100ug Lyophilized 100ul

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#39461010   2024/10/24 To Up

Tissue factor pathway inhibitor-2 inhibits integrin β1 activation and focal adhesion formation and suppresses peritoneal ovarian cancer dissemination in mice.

Tissue factor pathway inhibitor-2 (TFPI2) is a Kunitz-type serine protease inhibitor and an ovarian clear cell carcinoma (CCC) biomarker. TFPI2 is expressed in several cancers and exerts tumor-suppressive effects; however, the role of TFPI2 in the CCC cell phenotype remains unclear. Therefore, in this study, we investigated the function of TFPI2 by establishing a gene knockout (KO) in ES-2 CCC cells and observed the change in phenotypes in vitro and in vivo. TFPI2 KO inhibited ES-2 cell proliferation, increased extracellular matrix protein adhesion, enhanced focal adhesion formation and activated integrin β1 cell surface clustering in vitro, and markedly increased ES-2 tumor growth and dissemination in the peritoneal cavity of a mouse xenograft model. These findings suggest a novel function of TFPI2 expression in suppressing the formation of focal adhesions in CCC cells, potentially by activating integrin β1. This function plays a role in the peritoneal growth characteristics of CCC cells.
Yukihide Ota, Mari Uomoto, Shiro Koizume, Shinya Sato, Daisuke Hoshino, Mitsuyo Yoshihara, Yoshiyasu Nakamura, Hiroko Tadokoro, Shohei Myoba, Norihisa Ohtake, Etsuko Miyagi, Yohei Miyagi

2445 related Products with: Tissue factor pathway inhibitor-2 inhibits integrin β1 activation and focal adhesion formation and suppresses peritoneal ovarian cancer dissemination in mice.

100 μg

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#39456226   2024/10/12 To Up

The Formation of Stable Lung Tumor Spheroids during Random Positioning Involves Increased Estrogen Sensitivity.

The formation of tumor spheroids on the random positioning machine (RPM) is a complex and important process, as it enables the study of metastasis ex vivo. However, this process is not yet understood in detail. In this study, we compared the RPM-induced spheroid formation of two cell types of lung carcinoma (NCI-H1703 squamous cell carcinoma cells and Calu-3 adenocarcinoma cells). While NCI-H1703 cells were mainly present as spheroids after 3 days of random positioning, Calu-3 cells remained predominantly as a cell layer. We found that two-dimensional-growing Calu-3 cells have less mucin-1, further downregulate their expression on the RPM and therefore exhibit a higher adhesiveness. In addition, we observed that Calu-3 cells can form spheroids, but they are unstable due to an imbalanced ratio of adhesion proteins (β-integrin, E-cadherin) and anti-adhesion proteins (mucin-1) and are likely to disintegrate in the shear environment of the RPM. RPM-exposed Calu-3 cells showed a strongly upregulated expression of the estrogen receptor alpha gene . In the presence of 17β-estradiol or phenol red, more stable Calu-3 spheroids were formed, which was presumably related to an increased amount of E-cadherin in the cell aggregates. Thus, RPM-induced tumor spheroid formation depends not solely on cell-type-specific properties but also on the complex interplay between the mechanical influences of the RPM and, to some extent, the chemical composition of the medium used during the experiments.
Balkis Barkia, Viviann Sandt, Daniela Melnik, José Luis Cortés-Sánchez, Shannon Marchal, Bjorn Baselet, Sarah Baatout, Jayashree Sahana, Daniela Grimm, Markus Wehland, Herbert Schulz, Manfred Infanger, Armin Kraus, Marcus Krüger

1722 related Products with: The Formation of Stable Lung Tumor Spheroids during Random Positioning Involves Increased Estrogen Sensitivity.

100 U

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#39453784   2024/10/25 To Up

NAT10 promotes vascular remodelling via mRNA ac4C acetylation.

Vascular smooth muscle cell (VSMC) phenotype switching is a pathological hallmark in various cardiovascular diseases. N4-acetylcytidine (ac4C) catalyzed by N-acetyltransferase 10 (NAT10) is well conserved in the enzymatic modification of ribonucleic acid (RNA). NAT10-mediated ac4C acetylation is involved in various physiological and pathological processes, including cardiac remodelling. However, the biological functions and underlying regulatory mechanisms of mRNA ac4C modifications in vascular diseases remain elusive.
Cheng Yu, Yue Chen, Hao Luo, Weihong Lin, Xin Lin, Qiong Jiang, Hongjin Liu, Wenkun Liu, Jing Yang, Yu Huang, Jun Fang, Duofen He, Yu Han, Shuo Zheng, Hongmei Ren, Xuewei Xia, Junyi Yu, Lianglong Chen, Chunyu Zeng

1959 related Products with: NAT10 promotes vascular remodelling via mRNA ac4C acetylation.

50μg/vial100ug/vial5ug20μg/vial100 ug/vial10000 tests75мg/vial2ug x 20100ug/vial100μg/vial100 ug/vial

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