scholarly journals Microarray analysis to explore the effect of CXCL12 isoforms in a pancreatic pre-tumor cell model

2021 ◽  
Vol 27 (47) ◽  
pp. 8194-8198
Author(s):  
Yan-Dong Miao ◽  
Jiang-Tao Wang ◽  
Xiao-Long Tang ◽  
Deng-Hai Mi
Keyword(s):  
Tumor Cell ◽  
Microarray Analysis ◽  
Cell Model

scholarly journals Perk-Dependent Translational Regulation Promotes Tumor Cell Adaptation and Angiogenesis in Response to Hypoxic Stress

2006 ◽  
Vol 26 (24) ◽  
pp. 9517-9532 ◽  
Author(s):  
Jaime D. Blais ◽  
Christina L. Addison ◽  
Robert Edge ◽  
Theresa Falls ◽  
Huijun Zhao ◽  
...  
Keyword(s):  
Tumor Microenvironment ◽  
Tumor Cell ◽  
Microarray Analysis ◽  
Translational Control ◽  
Translational Regulation ◽  
Control Program ◽  
Cellular Adhesion ◽  
Dependent Manner ◽  
Hypoxic Stress ◽  
Cell Adaptation

ABSTRACT It has been well established that the tumor microenvironment can promote tumor cell adaptation and survival. However, the mechanisms that influence malignant progression have not been clearly elucidated. We have previously demonstrated that cells cultured under hypoxic/anoxic conditions and transformed cells in hypoxic areas of tumors activate a translational control program known as the integrated stress response (ISR). Here, we show that tumors derived from K-Ras-transformed Perk−/− mouse embryonic fibroblasts (MEFs) are smaller and exhibit less angiogenesis than tumors with an intact ISR. Furthermore, Perk promotes a tumor microenvironment that favors the formation of functional microvessels. These observations were corroborated by a microarray analysis of polysome-bound RNA in aerobic and hypoxic Perk+/+ and Perk−/− MEFs. This analysis revealed that a subset of proangiogenic transcripts is preferentially translated in a Perk-dependent manner; these transcripts include VCIP, an adhesion molecule that promotes cellular adhesion, integrin binding, and capillary morphogenesis. Taken with the concomitant Perk-dependent translational induction of additional proangiogenic genes identified by our microarray analysis, this study suggests that Perk plays a role in tumor cell adaptation to hypoxic stress by regulating the translation of angiogenic factors necessary for the development of functional microvessels and further supports the contention that the Perk pathway could be an attractive target for novel antitumor modalities.

scholarly journals HDAC Inhibition Counteracts Metastatic Re-Activation of Prostate Cancer Cells Induced by Chronic mTOR Suppression

Cells ◽  
2018 ◽  
Vol 7 (9) ◽  
pp. 129 ◽  
Author(s):  
Jasmina Makarević ◽  
Jochen Rutz ◽  
Eva Juengel ◽  
Sebastian Maxeiner ◽  
Jens Mani ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Tumor Cell ◽  
Cancer Cells ◽  
Cell Model ◽  
Close Association ◽  
Migration And Invasion ◽  
Hdac Inhibition ◽  
Prostate Cancer Cells ◽  
Metastatic Activity ◽  
Integrin Α5

This study was designed to investigate whether epigenetic modulation by histone deacetylase (HDAC) inhibition might circumvent resistance towards the mechanistic target of rapamycin (mTOR) inhibitor temsirolimus in a prostate cancer cell model. Parental (par) and temsirolimus-resistant (res) PC3 prostate cancer cells were exposed to the HDAC inhibitor valproic acid (VPA), and tumor cell adhesion, chemotaxis, migration, and invasion were evaluated. Temsirolimus resistance was characterized by reduced binding of PC3res cells to endothelium, immobilized collagen, and fibronectin, but increased adhesion to laminin, as compared to the parental cells. Chemotaxis, migration, and invasion of PC3res cells were enhanced following temsirolimus re-treatment. Integrin α and β receptors were significantly altered in PC3res compared to PC3par cells. VPA significantly counteracted temsirolimus resistance by down-regulating tumor cell–matrix interaction, chemotaxis, and migration. Evaluation of integrin expression in the presence of VPA revealed a significant down-regulation of integrin α5 in PC3res cells. Blocking studies demonstrated a close association between α5 expression on PC3res and chemotaxis. In this in vitro model, temsirolimus resistance drove prostate cancer cells to become highly motile, while HDAC inhibition reversed the metastatic activity. The VPA-induced inhibition of metastatic activity was accompanied by a lowered integrin α5 surface level on the tumor cells.

scholarly journals Two-Photon Imaging of the Interaction of mTORC1 Components using Fluorescence Energy Transfer between Gfp-Expressing Proteins in a Spheroid Tumor Cell Model

2014 ◽  
Vol 106 (2) ◽  
pp. 199a
Author(s):  
Christopher D. Stubbs ◽  
Kathrin M. Scherer ◽  
Anthony W. Parker ◽  
Eleanor C. Weston ◽  
Stanley W. Botchway
Keyword(s):  
Energy Transfer ◽  
Tumor Cell ◽  
Cell Model ◽  
Fluorescence Energy Transfer ◽  
Two Photon ◽  
Photon Imaging ◽  
Two Photon Imaging ◽  
Fluorescence Energy

Identification of liver metastasis-related genes in a novel human pancreatic carcinoma cell model by microarray analysis

2009 ◽  
Vol 283 (1) ◽  
pp. 84-91 ◽  
Author(s):  
Wei-Dong Shi ◽  
Zhi-Qiang Meng ◽  
Zhen Chen ◽  
Jun-Hua Lin ◽  
Zhen-Hua Zhou ◽  
...  
Keyword(s):  
Liver Metastasis ◽  
Pancreatic Carcinoma ◽  
Microarray Analysis ◽  
Carcinoma Cell ◽  
Cell Model ◽  
Human Pancreatic Carcinoma Cell

scholarly journals Discrimination between Breast Cancer Cells and White Blood Cells by Non-Invasive Measurements: Implications for a Novel In Vitro-Based Circulating Tumor Cell Model Using Digital Holographic Cytometry

2020 ◽  
Vol 10 (14) ◽  
pp. 4854
Author(s):  
Zahra El-Schich ◽  
Birgit Janicke ◽  
Kersti Alm ◽  
Nishtman Dizeyi ◽  
Jenny L. Persson ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Cell ◽  
Cancer Cells ◽  
Cell Lines ◽  
Blood Cells ◽  
Breast Cancer Cells ◽  
Cell Model ◽  
White Blood Cells ◽  
Circulating Tumor Cell

Breast cancer is the second most common cancer worldwide. Metastasis is the main reason for death in breast cancer, and today, there is a lack of methods to detect and isolate circulating tumor cells (CTCs), mainly due to their heterogeneity and rarity. There are some systems that are designed to detect rare epithelial cancer cells in whole blood based on the most common marker used today, the epithelial cell adhesion molecule (EpCAM). It has been shown that aggressive breast cancer metastases are of non-epithelial origin and are therefore not always detected using EpCAM as a marker. In the present study, we used an in vitro-based circulating tumor cell model comprising a collection of six breast cancer cell lines and white blood cell lines. We used digital holographic cytometry (DHC) to characterize and distinguish between the different cell types by area, volume and thickness. Here, we present significant differences in cell size-related parameters observed when comparing white blood cells and breast cancer cells by using DHC. In conclusion, DHC can be a powerful diagnostic tool for the characterization of CTCs in the blood.

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