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Changes in microfilament and focal adhesion distribution with loss of androgen responsiveness in cultured mammary tumor cells.

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Standard

Changes in microfilament and focal adhesion distribution with loss of androgen responsiveness in cultured mammary tumor cells. / Couchman, J R; Yates, J; King, R J; Badley, R A.

I: Cancer Research, Bind 41, Nr. 1, 1981, s. 263-9.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Couchman, JR, Yates, J, King, RJ & Badley, RA 1981, 'Changes in microfilament and focal adhesion distribution with loss of androgen responsiveness in cultured mammary tumor cells.', Cancer Research, bind 41, nr. 1, s. 263-9.

APA

Couchman, J. R., Yates, J., King, R. J., & Badley, R. A. (1981). Changes in microfilament and focal adhesion distribution with loss of androgen responsiveness in cultured mammary tumor cells. Cancer Research, 41(1), 263-9.

Vancouver

Couchman JR, Yates J, King RJ, Badley RA. Changes in microfilament and focal adhesion distribution with loss of androgen responsiveness in cultured mammary tumor cells. Cancer Research. 1981;41(1):263-9.

Author

Couchman, J R ; Yates, J ; King, R J ; Badley, R A. / Changes in microfilament and focal adhesion distribution with loss of androgen responsiveness in cultured mammary tumor cells. I: Cancer Research. 1981 ; Bind 41, Nr. 1. s. 263-9.

Bibtex

@article{f72a8fe0598f11dd8d9f000ea68e967b,
title = "Changes in microfilament and focal adhesion distribution with loss of androgen responsiveness in cultured mammary tumor cells.",
abstract = "The actin-containing microfilaments, microtubules, and fibronectin expression of Shionogi 115 mouse mammary tumor cells were visualized by indirect immunofluorescence microscopy. Also studied was the focal adhesion distribution as revealed by interference reflection microscopy and the ability of the cells to grow in suspension culture. All these parameters were documented for androgen-responsive and -unresponsive cells grown in culture, as well as the transition of androgen-responsive to -unresponsive cells when deprived of androgen. The androgen-unresponsive cells had extensive and prominent microfilament bundles together with focal adhesions on the lower cell surface and also showed strict anchorage dependence for growth. In contrast, microfilament bundles and focal adhesions were absent from androgen-responsive cells, which furthermore had the ability to grow in suspension culture. Differences were also apparent in fibronectin expression, the androgen-unresponsive cells having more of this glycoprotein detectable on their surfaces than the androgen-responsive cells. The androgen-responsive and -unresponsive cells had similar microtubule arrays, however. During the transition from the androgen-responsive to the androgen-unresponsive phenotype, the androgen-responsive cells gradually took on the characteristics of androgen-unresponsive cells as judged by cellular morphology or the presence of focal adhesions and microfilament bundles. At intermediate stages in this process, characteristics of both cell types were visible in the cell populations. However, at the stage where all androgen-responsive characteristics were lost, the cells were no longer androgen sensitive. The loss of androgen responsiveness in Shionogi 115 mouse mammary tumor cells is correlated with changes at the cell membrane and the microfilament component of the cytoskeleton.",
author = "Couchman, {J R} and J Yates and King, {R J} and Badley, {R A}",
note = "Keywords: Animals; Cell Adhesion; Cell Division; Cells, Cultured; Cytoskeleton; Female; Fibronectins; Mammary Neoplasms, Experimental; Mice; Microtubules; Receptors, Androgen; Receptors, Steroid; Testosterone",
year = "1981",
language = "English",
volume = "41",
pages = "263--9",
journal = "Cancer Research",
issn = "0008-5472",
publisher = "American Association for Cancer Research",
number = "1",

}

RIS

TY - JOUR

T1 - Changes in microfilament and focal adhesion distribution with loss of androgen responsiveness in cultured mammary tumor cells.

AU - Couchman, J R

AU - Yates, J

AU - King, R J

AU - Badley, R A

N1 - Keywords: Animals; Cell Adhesion; Cell Division; Cells, Cultured; Cytoskeleton; Female; Fibronectins; Mammary Neoplasms, Experimental; Mice; Microtubules; Receptors, Androgen; Receptors, Steroid; Testosterone

PY - 1981

Y1 - 1981

N2 - The actin-containing microfilaments, microtubules, and fibronectin expression of Shionogi 115 mouse mammary tumor cells were visualized by indirect immunofluorescence microscopy. Also studied was the focal adhesion distribution as revealed by interference reflection microscopy and the ability of the cells to grow in suspension culture. All these parameters were documented for androgen-responsive and -unresponsive cells grown in culture, as well as the transition of androgen-responsive to -unresponsive cells when deprived of androgen. The androgen-unresponsive cells had extensive and prominent microfilament bundles together with focal adhesions on the lower cell surface and also showed strict anchorage dependence for growth. In contrast, microfilament bundles and focal adhesions were absent from androgen-responsive cells, which furthermore had the ability to grow in suspension culture. Differences were also apparent in fibronectin expression, the androgen-unresponsive cells having more of this glycoprotein detectable on their surfaces than the androgen-responsive cells. The androgen-responsive and -unresponsive cells had similar microtubule arrays, however. During the transition from the androgen-responsive to the androgen-unresponsive phenotype, the androgen-responsive cells gradually took on the characteristics of androgen-unresponsive cells as judged by cellular morphology or the presence of focal adhesions and microfilament bundles. At intermediate stages in this process, characteristics of both cell types were visible in the cell populations. However, at the stage where all androgen-responsive characteristics were lost, the cells were no longer androgen sensitive. The loss of androgen responsiveness in Shionogi 115 mouse mammary tumor cells is correlated with changes at the cell membrane and the microfilament component of the cytoskeleton.

AB - The actin-containing microfilaments, microtubules, and fibronectin expression of Shionogi 115 mouse mammary tumor cells were visualized by indirect immunofluorescence microscopy. Also studied was the focal adhesion distribution as revealed by interference reflection microscopy and the ability of the cells to grow in suspension culture. All these parameters were documented for androgen-responsive and -unresponsive cells grown in culture, as well as the transition of androgen-responsive to -unresponsive cells when deprived of androgen. The androgen-unresponsive cells had extensive and prominent microfilament bundles together with focal adhesions on the lower cell surface and also showed strict anchorage dependence for growth. In contrast, microfilament bundles and focal adhesions were absent from androgen-responsive cells, which furthermore had the ability to grow in suspension culture. Differences were also apparent in fibronectin expression, the androgen-unresponsive cells having more of this glycoprotein detectable on their surfaces than the androgen-responsive cells. The androgen-responsive and -unresponsive cells had similar microtubule arrays, however. During the transition from the androgen-responsive to the androgen-unresponsive phenotype, the androgen-responsive cells gradually took on the characteristics of androgen-unresponsive cells as judged by cellular morphology or the presence of focal adhesions and microfilament bundles. At intermediate stages in this process, characteristics of both cell types were visible in the cell populations. However, at the stage where all androgen-responsive characteristics were lost, the cells were no longer androgen sensitive. The loss of androgen responsiveness in Shionogi 115 mouse mammary tumor cells is correlated with changes at the cell membrane and the microfilament component of the cytoskeleton.

M3 - Journal article

C2 - 7192599

VL - 41

SP - 263

EP - 269

JO - Cancer Research

JF - Cancer Research

SN - 0008-5472

IS - 1

ER -

ID: 5167938