scholarly journals Negative regulation between the expression levels of receptor for hyaluronic acid‑mediated motility and hyaluronan leads to cell migration in pancreatic cancer

2020 ◽  
Vol 20 (5) ◽  
pp. 1-1
Author(s):  
Xiao-Bo Cheng ◽  
Shuwen Wang ◽  
Hua Yang ◽  
Hanxing Tong ◽  
Guodong Shi ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Migration ◽  
Hyaluronic Acid ◽  
Negative Regulation ◽  
Expression Levels

scholarly journals MicroRNA-301a-3p promotes pancreatic cancer progression via negative regulation ofSMAD4

Oncotarget ◽  
2015 ◽  
Vol 6 (25) ◽  
pp. 21046-21063 ◽  
Author(s):  
Xiang Xia ◽  
Kundong Zhang ◽  
Gang Cen ◽  
Tao Jiang ◽  
Jun Cao ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Progression ◽  
Negative Regulation

scholarly journals Collagen Organization Does Not Influence T-Cell Distribution in Stroma of Human Pancreatic Cancer

Cancers ◽  
2021 ◽  
Vol 13 (15) ◽  
pp. 3648
Author(s):  
Eva-Maria Kamionka ◽  
Baifeng Qian ◽  
Wolfgang Gross ◽  
Frank Bergmann ◽  
Thilo Hackert ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
T Cells ◽  
Cell Migration ◽  
T Cell ◽  
Human Pancreatic Cancer ◽  
Ductal Adenocarcinoma ◽  
Cell Distribution ◽  
Collagen Organization ◽  
T Cell Migration ◽  
Collagen Alignment

The dominant intrastromal T-cell infiltration in pancreatic cancer is mainly caused by the contact guidance through the excessive desmoplastic reaction and could represent one of the obstacles to an effective immune response in this tumor type. This study analyzed the collagen organization in normal and malignant pancreatic tissues as well as its influence on T-cell distribution in pancreatic cancer. Human pancreatic tissue was analyzed using immunofluorescence staining and multiphoton and SHG microscopy supported by multistep image processing. The influence of collagen alignment on activated T-cells was studied using 3D matrices and time-lapse microscopy. It was found that the stroma of malignant and normal pancreatic tissues was characterized by complex individual organization. T-cells were heterogeneously distributed in pancreatic cancer and there was no relationship between T-cell distribution and collagen organization. There was a difference in the angular orientation of collagen alignment in the peritumoral and tumor-cell-distant stroma regions in the pancreatic ductal adenocarcinoma tissue, but there was no correlation in the T-cell densities between these regions. The grade of collagen alignment did not influence the directionality of T-cell migration in the 3D collagen matrix. It can be concluded that differences in collagen organization do not change the spatial orientation of T-cell migration or influence stromal T-cell distribution in human pancreatic cancer. The results of the present study do not support the rationale of remodeling of stroma collagen organization for improvement of T-cell–tumor cell contact in pancreatic ductal adenocarcinoma.

scholarly journals Snail Recruits Ring1B to Mediate Transcriptional Repression and Cell Migration in Pancreatic Cancer Cells

2014 ◽  
Vol 74 (16) ◽  
pp. 4353-4363 ◽  
Author(s):  
Jiangzhi Chen ◽  
Hong Xu ◽  
Xiuqun Zou ◽  
Jiamin Wang ◽  
Yi Zhu ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Migration ◽  
Cancer Cells ◽  
Transcriptional Repression ◽  
Pancreatic Cancer Cells

scholarly journals Identification of Key Deregulated RNA-Binding Proteins in Pancreatic Cancer by Meta-Analysis and Prediction of Their Role as Modulators of Oncogenesis

2021 ◽  
Vol 9 ◽  
Author(s):  
Moumita Mukherjee ◽  
Srikanta Goswami
Keyword(s):  
Pancreatic Cancer ◽  
Cell Migration ◽  
Binding Proteins ◽  
Rna Binding ◽  
Rna Binding Proteins ◽  
Meta Analysis ◽  
Enrichment Analysis ◽  
Pathway Enrichment Analysis ◽  
Ppi Network ◽  
Pathway Enrichment

RNA-binding proteins (RBPs) play a significant role in multiple cellular processes with their deregulations strongly associated with cancer. However, there are not adequate evidences regarding global alteration and functions of RBPs in pancreatic cancer, interrogated in a systematic manner. In this study, we have prepared an exhaustive list of RBPs from multiple sources, downloaded gene expression microarray data from a total of 241 pancreatic tumors and 124 normal pancreatic tissues, performed a meta-analysis, and obtained differentially expressed RBPs (DE-RBPs) using the Limma package of R Bioconductor. The results were validated in microarray datasets and the Cancer Genome Atlas (TCGA) RNA sequencing dataset for pancreatic adenocarcinoma (PAAD). Pathway enrichment analysis was performed using DE-RBPs, and we also constructed the protein–protein interaction (PPI) network to detect key modules and hub-RBPs. Coding and noncoding targets for top altered and hub RBPs were identified, and altered pathways modulated by these targets were also investigated. Our meta-analysis identified 45 upregulated and 15 downregulated RBPs as differentially expressed in pancreatic cancer, and pathway enrichment analysis demonstrated their important contribution in tumor development. As a result of PPI network analysis, 26 hub RBPs were detected and coding and noncoding targets for all these RBPs were categorized. Functional exploration characterized the pathways related to epithelial-to-mesenchymal transition (EMT), cell migration, and metastasis to emerge as major pathways interfered by the targets of these RBPs. Our study identified a unique meta-signature of 26 hub-RBPs to primarily modulate pancreatic tumor cell migration and metastasis in pancreatic cancer. IGF2BP3, ISG20, NIP7, PRDX1, RCC2, RUVBL1, SNRPD1, PAIP2B, and SIDT2 were found to play the most prominent role in the regulation of EMT in the process. The findings not only contribute to understand the biology of RBPs in pancreatic cancer but also to evaluate their candidature as possible therapeutic targets.

scholarly journals ANLN Promotes Cell Migration and Invasion Through RhoA-ROCK Signaling in Cervical Cancer

2021 ◽  
Author(s):  
Congzhe Hou ◽  
Zhen Liang ◽  
Yongxia Yang ◽  
Yunhai Yu ◽  
Tingting Liang ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cell Proliferation ◽  
Cell Migration ◽  
Stress Fiber ◽  
Actin Binding ◽  
Migration And Invasion ◽  
Actin Stress Fiber ◽  
Western Blots ◽  
Expression Levels ◽  
Cell Migration And Invasion

IntroductionAnillin actin binding protein (ANLN) is involved in various human cancers. It is often upregulated in various cancers, including cervical cancer (CC). however, the exact role of ANLN in the modulation of CC and the underlying molecular mechanism remain unknown. In this study, we aimed to investigate the effects of ANLN on the proliferation, migration, and invasion of CC cells, as well as determine the molecular mechanisms underlying these effects.Material and methodsANLN expression levels were analyzed in normal cervical and CC specimens using public databases and tissue samples. The prognosis was determined using TCGA database. Cell proliferation, migration and invasion were measured by Edu assay, wound-healing assay and transwell assay, respectively. Immunofluorescence was used to examined the influence actin stress fiber integrity caused by ANLN inhibition. Western blots were used to measure the protein expression.ResultsANLN expression levels in CC were higher than those in normal tissues, and ANLN overexpression was highly correlated with poor prognosis. ANLN knockdown inhibited CC cell proliferation, migration, and invasion in vitro, while ANLN overexpression exerted an inverse biological phenotype. Immunofluorescence showed that ANLN inhibition could influence actin stress fiber integrity. ANLN expression was positively correlated with ROCK1 and ROCK2 expression in CC. Overexpression of ANLN activated RhoA and upregulated ROCK1 and ROCK2. Furthermore, ROCK1 and ROCK2 expression levels were also impeded by Y27632, which is a specific inhibitor of RhoA. They also weakened the migration and invasion ability in ANLN overexpression HeLa cells.ConclusionsANLN promotes cell migration and invasion through RhoA-ROCK signaling in CC.

scholarly journals Expression levels of microRNA-375 in pancreatic cancer

2013 ◽  
Vol 1 (3) ◽  
pp. 393-398 ◽  
Author(s):  
SHIDUO SONG ◽  
JIAN ZHOU ◽  
SONGBING HE ◽  
DONGMING ZHU ◽  
ZIXIANG ZHANG ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Expression Levels

CD44-dependent lymphoma cell dissemination: a cell surface CD44 variant, rather than standard CD44, supports in vitro lymphoma cell rolling on hyaluronic acid substrate and its in vivo accumulation in the peripheral lymph nodes

2001 ◽  
Vol 114 (19) ◽  
pp. 3463-3477
Author(s):  
Shulamit B. Wallach-Dayan ◽  
Valentin Grabovsky ◽  
Jürgen Moll ◽  
Jonathan Sleeman ◽  
Peter Herrlich ◽  
...  
Keyword(s):  
Cell Migration ◽  
Hyaluronic Acid ◽  
Lymph Node ◽  
Cell Surface ◽  
Lymph Nodes ◽  
Local Tumor ◽  
Cd44 Variant ◽  
Peripheral Lymph

Cell motility is an essential element of tumor dissemination, allowing organ infiltration by cancer cells. Using mouse LB lymphoma cells transfected with standard CD44 (CD44s) cDNA (LB-TRs cells) or with the alternatively spliced CD44 variant CD44v4-v10 (CD44v) cDNA (LB-TRv cells), we explored their CD44-dependent cell migration. LB-TRv cells, but not LB-TRs or parental LB cells, bound soluble hyaluronic acid (HA) and other glycosaminoglycans (GAGs), and exclusively formed, under physiological shear force, rolling attachments on HA substrate. Furthermore, LB-TRv cells, but not LB-TRs cells or their parental LB cells, displayed accelerated local tumor formation and enhanced accumulation in the peripheral lymph nodes after s.c. inoculation. The aggressive metastatic behavior of i.v.-injected LB-TRV cells, when compared with that of other LB-transfectants, is attributed to more efficient migration to the lymph nodes, rather than to local growth in the lymph node. Injection of anti-CD44 monoclonal antibody or of the enzyme hyaluronidase also prevented tumor growth in lymph nodes of BALB/c mice inoculated with LB-TRv cells. The enhanced in vitro rolling and enhanced in vivo local tumor growth and lymph node invasion disappeared in LB cells transfected with CD44v cDNA bearing a point mutation at the HA binding site, located at the distal end of the molecule constant region. These findings show that the interaction of cell surface CD44v with HA promotes cell migration both in vitro and in vivo, and they contribute to our understanding of the mechanism of cell trafficking, including tumor spread.

Sign in / Sign up

Export Citation Format

Share Document