Activin inhibits basal and androgen-stimulated proliferation and induces apoptosis in the human prostatic cancer cell line, LNCaP

Endocrinology
Q F WangP M Sluss

Abstract

LNCaP cells, derived from an androgen-sensitive cell line widely employed as an in vitro model of human prostate cancer, have been shown to express activin receptors. Activin is a local regulator of cellular growth, appears to play a key role in mesoderm induction and differentiation during development, and has been implicated in gonadal tumorigenesis. Follistatin, a monomeric glycoprotein that specifically binds and neutralizes activin, is often coexpressed with activin and, thus, modulates the autocrine/paracrine biological activity of this potent growth factor. We tested the hypothesis that LNCaP growth is modulated by the activin/follistatin system. Recombinant human activin A inhibited [3H]thymidine incorporation in a dose-dependent fashion with an ED50 of approximately 0.43 +/- 0.3 nM. Activin (0.1-3 nM) also inhibited dihydrotestosterone (DHT)-stimulated [3H]thymidine incorporation in LNCaP cells. Similarly, recombinant human inhibin A inhibited LNCaP proliferation, but was only 1/100th as potent as activin. Furthermore, activin (3 nM) induced a 3-fold increase in the extent of labeling of low mol wt DNA fragments typical of apoptosis. Activin-induced apoptosis was also indicated by an increase in the number of cells wit...Continue Reading

Citations

Mar 15, 2001·Proceedings of the National Academy of Sciences of the United States of America·G H SuS E Kern
Jan 5, 2002·Proceedings of the National Academy of Sciences of the United States of America·Dorry L SegevShyamala Maheswaran
Aug 24, 2001·Developmental Biology·B CancillaG P Risbridger
Nov 20, 2012·Biochemical and Biophysical Research Communications·Masatoshi NomuraRyoichi Takayanagi
Oct 4, 2016·Biochemical and Biophysical Research Communications·Rui LiuSa-Ouk Kang
Feb 6, 2004·American Journal of Physiology. Endocrinology and Metabolism·Yasuhisa FujiiKazunori Kihara
Oct 21, 2004·Cancer·David G BostwickBarry Timms
Feb 28, 2003·Biology of Reproduction·Christian TessierGeula Gibori
Dec 13, 2018·Physiological Reviews·Enrrico BloiseFernando M Reis
Dec 20, 2003·Molecular Endocrinology·Jennifer L CareyShyamala Maheswaran
Jan 31, 2002·Molecular Endocrinology·Daniel J BernardTeresa K Woodruff
Jun 8, 2004·The Journal of Clinical Endocrinology and Metabolism·Ki-Yon KimPeter C K Leung
Nov 11, 2009·Current Eye Research·Chikako KannoHidetoshi Yamashita
Jul 5, 2013·American Journal of Physiology. Renal Physiology·Mandeep SinghAlexei G Basnakian
Dec 12, 2001·Endocrine Reviews·G P RisbridgerD M Robertson
Oct 5, 2002·The Journal of Clinical Endocrinology and Metabolism·Daniel C DanilaAnne Klibanski
Jan 30, 2002·Experimental Biology and Medicine·Ye-Guang ChenShao-Yao Ying
Aug 27, 2005·The Journal of Biological Chemistry·Guangchun ChenHajime Nawata
Dec 21, 2002·The Journal of Biological Chemistry·Ezra Wiater, Wylie Vale
Mar 27, 1999·Biochemical and Biophysical Research Communications·S Lin, S Y Ying

❮ Previous
Next ❯

Related Concepts

Related Feeds

Apoptosis in Cancer

Apoptosis is an important mechanism in cancer. By evading apoptosis, tumors can continue to grow without regulation and metastasize systemically. Many therapies are evaluating the use of pro-apoptotic activation to eliminate cancer growth. Here is the latest research on apoptosis in cancer.

Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis