Activation of Mitogen-Activated Protein Kinases Is Required for α1-Adrenergic Agonist-Induced Cell Scattering in Transfected HepG2 Cells

Spector, Mark S.; Nguyễn, Vân Hà; Sheng, Xuening; He, Liusheng; Woodward, John J.; Fan, Songqing; Baumgarten, Clive M.; Kunos, George; Dent, Paul; Gao, Bin

doi:10.1006/excr.2000.4907

Cited by 18 publications

(13 citation statements)

References 52 publications

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Section: Discussionmentioning

confidence: 99%

“…However, recent studies have reported an anti-proliferative effect of ␣ 1 -AR activation in certain cell types (27)(28)(29). In the process of hepatic regeneration after hepatectomy, ␣ 1 -AR stimulation is thought to act as anti-proliferative signal in hepatic cells (28,29). Also, it was reported that the activation of ␣ 1 B-AR in HepG2 human hepatoma cells stably transfected with a rat ␣ 1 B-AR cDNA inhibited cell growth via a p42 MAPK and p21 WAF1/CIP1 -dependent mechanism (28).…”

Section: Discussionmentioning

confidence: 99%

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α1-Adrenergic Receptor Subtypes Differentially Control the Cell Cycle of Transfected CHO Cells through a cAMP-dependent Mechanism Involving p27

Shibata

Katsuma

Koshimizu

et al. 2003

Journal of Biological Chemistry

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

α1-Adrenergic Receptor Subtypes Differentially Control the Cell Cycle of Transfected CHO Cells through a cAMP-dependent Mechanism Involving p27

Shibata

Katsuma

Koshimizu

et al. 2003

Journal of Biological Chemistry

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“…As shown in Figure 3, PC-3 cells could be "lighted up" after being incubated with 1d (1 μM), while HepG2 cells (low α 1 -AR expression) showed little fluorescence. 27 Also, 1d shows high displaceable properties in PC-3 prostate cancer cells with doxazosin. These findings confirm probe 1d as a labeling tool in α 1 -AR overexpressing cells.…”

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confidence: 95%

Discovery of Quinazoline-Based Fluorescent Probes to α₁-Adrenergic Receptors

Zhang

et al. 2015

ACS Med. Chem. Lett.

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α 1 -Adrenergic receptors (α 1 -ARs), as the essential members of G protein-coupled receptors (GPCRs), can mediate numerous physiological responses in the sympathetic nervous system. In the current research, a series of quinazoline-based small-molecule fluorescent probes to α 1 -ARs (1a−1e), including two parts, a pharmacophore for α 1 -AR recognition and a fluorophore for visualization, were well designed and synthesized. The biological evaluation results displayed that these probes held reasonable fluorescent properties, high affinity, accepted cell toxicity, and excellent subcellular localization imaging potential for α 1 -ARs.

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“…Epidermal growth factor receptor (EGFR) signaling has been linked to tumor growth and malignant progression (1)(2)(3)(4)(5)(6)(7). EGFR is one of four members of the ErbB family of receptors.…”

Section: Introductionmentioning

confidence: 99%

A Novel Mechanism of Resistance to Epidermal Growth Factor Receptor Antagonism In vivo

et al. 2007

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Epidermal growth factor receptor (EGFR) is widely expressed in a number of solid tumors including colorectal cancers. Overexpression of this receptor is one means by which a cell can achieve positive signals for survival and proliferation; another effective means is by constitutive activation of EGFR. We have elucidated the role of constitutive EGFR signaling in malignant progression by stably transfecting colon cancer cells with a human transforming growth factor-A cDNA (a ligand for EGFR) under repressible control by tetracycline. We show that constitutive expression of transforming growth factor-A and its subsequent constitutive activation of EGFR allows for cancer cell survival in response to environmental stress in vitro and in vivo as well. The reversal of constitutive EGFR activation results in the loss of downstream mitogenactivated protein kinase and Akt activation, and a reduction in xenograft size that is associated with decreased proliferation and increased apoptosis. We used CI-1033, a small molecule antagonist of EGFR, to dissect an activation pathway that shows the ability of ERBb2 to activate Akt, but not Erk in the face of EGFR antagonism. This novel escape mechanism is a possible explanation of why anti-EGFR therapies have shown disappointing results in clinical trials. [Cancer Res 2007;67(2):665-73]

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Activation of Mitogen-Activated Protein Kinases Is Required for α1-Adrenergic Agonist-Induced Cell Scattering in Transfected HepG2 Cells

Cited by 18 publications

References 52 publications

α1-Adrenergic Receptor Subtypes Differentially Control the Cell Cycle of Transfected CHO Cells through a cAMP-dependent Mechanism Involving p27

α1-Adrenergic Receptor Subtypes Differentially Control the Cell Cycle of Transfected CHO Cells through a cAMP-dependent Mechanism Involving p27

Discovery of Quinazoline-Based Fluorescent Probes to α₁-Adrenergic Receptors

A Novel Mechanism of Resistance to Epidermal Growth Factor Receptor Antagonism In vivo

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Activation of Mitogen-Activated Protein Kinases Is Required for α1-Adrenergic Agonist-Induced Cell Scattering in Transfected HepG2 Cells

Cited by 18 publications

References 52 publications

α1-Adrenergic Receptor Subtypes Differentially Control the Cell Cycle of Transfected CHO Cells through a cAMP-dependent Mechanism Involving p27

α1-Adrenergic Receptor Subtypes Differentially Control the Cell Cycle of Transfected CHO Cells through a cAMP-dependent Mechanism Involving p27

Discovery of Quinazoline-Based Fluorescent Probes to α1-Adrenergic Receptors

A Novel Mechanism of Resistance to Epidermal Growth Factor Receptor Antagonism In vivo

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Discovery of Quinazoline-Based Fluorescent Probes to α₁-Adrenergic Receptors