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Fenretinide: induction of apoptosis and endogenous transforming growth factor beta in PC-3 prostate cancer cells.

Publication ,  Journal Article
Roberson, KM; Penland, SN; Padilla, GM; Selvan, RS; Kim, CS; Fine, RL; Robertson, CN
Published in: Cell Growth Differ
January 1997

N-(4-Hydroxyphenyl)retinamide (4-HPR, Fenretinide) is a retinoid derivative with antineoplastic activity in various tumor types including prostate carcinoma. The mechanism of action of 4-HPR toxicity is unknown. 4-HPR induces apoptosis in leukemia- and lymphoma-derived cells, neuroblastoma, and small cell lung cancers. The present study was designed to investigate: (a) the mechanism of 4-HPR cytotoxicity in prostate cancer cells; and (b) correlate increased expression of transforming growth factor beta 1 (TGF beta 1) with induction of apoptosis. 4-HPR exposure to PC-3 cells in vitro was associated with apoptosis as evidenced by increased incidence of hypodiploid nuclei in propidium iodide fluorescence histograms and DNA fragmentation. An increase in the percentage of nuclei in the G1 phase of the cell cycle preceded induction of apoptosis. TGF beta 1-increased expression was noted in mRNA levels and in secretion of active TGF beta 1 into culture media. TGF beta 1 and TGF-beta receptor type II detected immunohistochemically were increased in 4-HPR-treated PC-3 cells. Furthermore, 4-HPR-induced cytotoxicity in PC-3 cells was abrogated by the addition of anti-TGF beta 1 antibody. In BT-20 cells, a 4-HPR-resistant breast carcinoma cell line, apoptosis was not observed after exposure to 4-HPR nor was TGF beta 1 expression enhanced in stained cells or in conditioned media. It is concluded that 4-HPR induces the expression of TGF beta 1 in association with the induction of apoptosis.

Duke Scholars

Published In

Cell Growth Differ

ISSN

1044-9523

Publication Date

January 1997

Volume

8

Issue

1

Start / End Page

101 / 111

Location

United States

Related Subject Headings

  • Tumor Cells, Cultured
  • Transforming Growth Factor beta
  • Time Factors
  • Receptors, Transforming Growth Factor beta
  • Receptor, Transforming Growth Factor-beta Type II
  • Protein Serine-Threonine Kinases
  • Prostatic Neoplasms
  • Oncology & Carcinogenesis
  • Male
  • Immunohistochemistry
 

Citation

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Roberson, K. M., Penland, S. N., Padilla, G. M., Selvan, R. S., Kim, C. S., Fine, R. L., & Robertson, C. N. (1997). Fenretinide: induction of apoptosis and endogenous transforming growth factor beta in PC-3 prostate cancer cells. Cell Growth Differ, 8(1), 101–111.
Roberson, K. M., S. N. Penland, G. M. Padilla, R. S. Selvan, C. S. Kim, R. L. Fine, and C. N. Robertson. “Fenretinide: induction of apoptosis and endogenous transforming growth factor beta in PC-3 prostate cancer cells.Cell Growth Differ 8, no. 1 (January 1997): 101–11.
Roberson KM, Penland SN, Padilla GM, Selvan RS, Kim CS, Fine RL, et al. Fenretinide: induction of apoptosis and endogenous transforming growth factor beta in PC-3 prostate cancer cells. Cell Growth Differ. 1997 Jan;8(1):101–11.
Roberson, K. M., et al. “Fenretinide: induction of apoptosis and endogenous transforming growth factor beta in PC-3 prostate cancer cells.Cell Growth Differ, vol. 8, no. 1, Jan. 1997, pp. 101–11.
Roberson KM, Penland SN, Padilla GM, Selvan RS, Kim CS, Fine RL, Robertson CN. Fenretinide: induction of apoptosis and endogenous transforming growth factor beta in PC-3 prostate cancer cells. Cell Growth Differ. 1997 Jan;8(1):101–111.

Published In

Cell Growth Differ

ISSN

1044-9523

Publication Date

January 1997

Volume

8

Issue

1

Start / End Page

101 / 111

Location

United States

Related Subject Headings

  • Tumor Cells, Cultured
  • Transforming Growth Factor beta
  • Time Factors
  • Receptors, Transforming Growth Factor beta
  • Receptor, Transforming Growth Factor-beta Type II
  • Protein Serine-Threonine Kinases
  • Prostatic Neoplasms
  • Oncology & Carcinogenesis
  • Male
  • Immunohistochemistry