Localization and Distribution of Actin Fibers in Normal, Transformed and Revertant Cells

Weber, Klaus; Lazarides, Elias; Goldman, Robert D.; Vogel, A; Pollack, Robert

doi:10.1101/sqb.1974.039.01.047

Cited by 69 publications

(52 citation statements)

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“…Studies using fluorescent antibody directed against actin showed that the arrangement of actin filaments in cables is lost or much reduced in mouse and rat cells transformed by simian virus 40 (10)(11)(12). McNutt et al (13,14) had drawn a similar conclusion from their earlier results using transmission electron microscopy.…”

supporting

confidence: 67%

Changes in microfilament organization and surface topogrophy upon transformation of chick embryo fibroblasts with Rous sarcoma virus.

Wang¹,

Goldberg²

1976

Proc. Natl. Acad. Sci. U.S.A.

159

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A series of morphological changes occurred when chick embryo fibroblasts infected with the NY68 mutant of Rous sarcoma virus were shifted from nonpermissive temperature (410) to permissive temperature (370). We observed three distinct stages in cell morphology and surface topography that were correlated with a reduction in the organization and assembly of actin-containing microfilament bundles. Our observations suggest that control of microfilament organization and surface topography are responsive to the presence of a functioning transforming gene (src) product of Rous sarcoma virus.Transformation of chick embryo fibroblasts by Rous sarcoma virus is independent of virus replication (1, 2) and is under the influence of a viral gene that is called the src gene because it contains sequences specific for sarcomagenesis (3). Cells infected with virus mutants that have a temperature-sensitive lesion in the src gene product are transformed at a permissive temperature but not at a nonpermissive temperature. Thermal denaturation of the src gene product of some of these mutants is reversible and thus provides a useful system for studying changes in cell metabolism that are associated with transformation.The presence of a functional src gene can be correlated with a broad array of alterations (2), many of which involve the membrane. Included in this category of membrane-associated phenomena in transformed cells are increased agglutinability with plant lectins, loss of surface proteins, changes in adhesion properties, changes in contact inhibition of growth and locomotion, changes in membrane transport, elevated levels of a protease that is a plasminogen activator, and changes in cell morphology. In particular, alteration in cell shape has been used as a convenient marker for assaying cellular transformation (4-6). Changes in the morphology and surface topography of mammalian cells are associated with the assembly and organization of cytoplasmic fibers such as microtubules, 100 A filaments, and microfilament bundles (7-9).The cytoskeleton of transformed cell lines seems to be altered (7, 9). Studies using fluorescent antibody directed against actin showed that the arrangement of actin filaments in cables is lost or much reduced in mouse and rat cells transformed by simian virus 40 (10-12). McNutt et al. (13,14) had drawn a similar conclusion from their earlier results using transmission electron microscopy. In the present study we describe changes in cell shape, topography, and cytoplasmic fibers in chick cells infected with Rous sarcoma virus that are associated with the action, either direct or indirect, of the src gene product. MATERIALS AND METHODSCells and Viruses. The growth and maintenance of normal and virus-infected chick embryo fibroblasts was as described (15). In all experiments, cultures were grown in Scherer's medium containing 10% tryptose phosphate broth and 5% calf serum. The temperature-sensitive transformation mutant NY68 of the Schmidt-Ruppin strain of Rous sarcoma virus was obtained from Drs. K...

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supporting

confidence: 67%

Changes in microfilament organization and surface topogrophy upon transformation of chick embryo fibroblasts with Rous sarcoma virus.

Wang¹,

Goldberg²

1976

Proc. Natl. Acad. Sci. U.S.A.

159

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“…However, at higher dosage levels (1/2 of IC 50 or 1548.5 nmol/L), the adhesion complex formation slightly decreased instead (but was still higher than the untreated control), which may be related to anoikis (or detachment-associated apoptosis). Actin was first identified in nonmuscle cells only f3 decades ago, and at the same time, it was found that actin filaments were disrupted in the malignant transformed cells (22). Actin is a ubiquitous protein present in all eukaryotic cells and is one of the major structural and functional proteins involved in maintaining cell morphology, cell adhesion, cell movement (motility), exocytosis and endocytosis, as well as cell division (23 -25).…”

Section: Discussionmentioning

confidence: 99%

Effect of an epidermal growth factor receptor tyrosine kinase inhibitor on actin remodeling in anin vitrobladder cancer carcinogenesis model

Jin¹,

Iwata

Belldegrun

et al. 2006

Molecular Cancer Therapeutics

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Alteration of actin remodeling is a marker of malignantassociated field defect and a potential surrogate biomarker for chemoprevention trials. We tested erlotinib, a specific tyrosine kinase inhibitor of epidermal growth factor receptor (EGFR), on actin remodeling in a bladder carcinogenic model consisting of untransformed HUC-PC cells and transformed MC-T11 cells, both derived from the same normal human urothelial clone immortalized by SV40. Erlotinib had a selective growth inhibitory and actin remodeling effect on MC-T11 cells over HUC-PC cells, as examined by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and immunofluorescence labeling with laser scan cytometer analysis, respectively. The IC 50 of untransformed HUC-PC cells was significantly higher than that of transformed MC-T11 cells (P < 0.05, t test). The actin remodeling effect was more prominent at lower dosage levels (1/8-1/4 of IC 50 ), which was accompanied by an increased cell adhesion and decreased motility. At higher dosage levels (1/2 of IC 50 ), erlotinib induced a decreased adhesion and anoikis (detachmentassociated apoptosis). The transformed MC-T11, but not HUC-PC, showed a weak constitutive EGFR phosphorylation activity, which was inhibited by erlotinib in a doseresponse manner. However, on epidermal growth factor stimulation, both cell lines showed a similar dose-response inhibitory effect on phosphorylated EGFR and mitogenactivated protein kinase (MAPK; P44/P42) activities, and MAPK inhibitor PD98059 showed no specific effect on erlotinib-induced actin remodeling, suggesting that pathways other than MAPK (P44/P42) may be responsible for erlotinib-induced actin remodeling. The findings provide evidence to support erlotinib-based bladder cancer chemoprevention and using actin remodeling as a marker for erlotinib-based intervention trials.

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“…Cytoskeletal actin is a ubiquitous protein present in all eukaryotic cells. 22 The cytoskeletal network is mainly composed of actin filaments, microtubules, intermediate filaments, and accessory proteins. As one of the major proteins in the cell, actin and its associated proteins play an important structural and functional roles, such as maintaining cell morphology, cell adhesion, cell motility, exo and endocytosis, and cell division.…”

Section: Discussionmentioning

confidence: 99%

Green tea induces annexin-I expression in human lung adenocarcinoma A549 cells: involvement of annexin-I in actin remodeling

Jin

Zhang

et al. 2007

Laboratory Investigation

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Green tea polyphenols exhibit multiple antitumor activities in various in vitro and in vivo tumor models, and the mechanisms of action are not clear. Previously, we found that green tea extract (GTE) regulates actin remodeling in different cell culture systems. Actin remodeling plays an important role in cancer cell morphology, cell adhesion, motility, and invasion. Using proteomic approaches, we found GTE-induced expression of annexin-I, a multifunctional actin binding protein, in these cell lines. In this study, we aimed to further define the functional role of GTE-induced annexin-I expression in actin remodeling, cell adhesion, and motility in lung adenocarcinoma A549 cells. We found that GTE stimulates the expression of annexin-I in a dose-dependent fashion. The GTE-induced annexin-I expression appears to be at the transcription level, and the increased annexin-I expression mediates actin polymerization, resulting in enhanced cell adhesion and decreased motility. Annexin-I specific interference resulted in loss of GTE-induced actin polymerization and cell adhesion, but not motility. In fact, annexin-I specific interference itself inhibited motility even without GTE. Together, annexin-I plays an important role in GTE-induced actin remodeling, and it may serve as a potential molecular target associated with the anticancer activities of green tea.

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Localization and Distribution of Actin Fibers in Normal, Transformed and Revertant Cells

Cited by 69 publications

References 0 publications

Changes in microfilament organization and surface topogrophy upon transformation of chick embryo fibroblasts with Rous sarcoma virus.

Changes in microfilament organization and surface topogrophy upon transformation of chick embryo fibroblasts with Rous sarcoma virus.

Effect of an epidermal growth factor receptor tyrosine kinase inhibitor on actin remodeling in anin vitrobladder cancer carcinogenesis model

Green tea induces annexin-I expression in human lung adenocarcinoma A549 cells: involvement of annexin-I in actin remodeling

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