Divergent effects of retinoic acids on the expression of ERalpha and 17beta-hydroxysteroid dehydrogenase type 2 in endometrial carcinoma cells (RL 95-2)

J Clin Endocrinol Metab. 2002 Feb;87(2):640-9. doi: 10.1210/jcem.87.2.8208.


The effects of E2 are dependent on ERs and local E2 concentration in target cells. Modulation of intracellular E2 concentration involves the action of 17beta-hydroxysteroid dehydrogenase (17HSD) type 2, the enzyme converting E2 to estrone. In the present study, the influence of RAs on the growth of endometrial cancer cell line RL 95-2 as well as the expression of ERs and 17HSD type 2 have been investigated. It was found that RAs repress the growth of RL 95-2 cells, which express all subtypes of RXR and RAR, as examined by RT-PCR. Also, quantitative RT-PCR analysis showed that both ERalpha and ERbeta are present in RL 95-2 cells, and Western blot assay further revealed that ERalpha expression was decreased by all trans-RA treatment. In contrast, RAs induced 17HSD type 2 mRNA expression in a dose- and time-dependent fashion. This stimulatory effect was also detected at the level of in vivo oxidative 17HSD activity in cultured cells. On the other hand, the abundance of 17HSD type 2 mRNA was not altered by RAs in cultured normal epithelial cells isolated from human early- and late-secretory endometrium. The data indicate that RAs have an inhibitory effect on the growth of RL 95-2 cells and a cross-talk with the estrogen pathway in estrogen-responsive endometrial cancer cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 17-Hydroxysteroid Dehydrogenases / genetics
  • 17-Hydroxysteroid Dehydrogenases / metabolism*
  • Carcinoma / metabolism*
  • Carcinoma / pathology
  • Cell Division / drug effects
  • Cells, Cultured
  • Endometrial Neoplasms / metabolism*
  • Endometrial Neoplasms / pathology
  • Estrogen Receptor alpha
  • Estrogen Receptor beta
  • Female
  • Humans
  • Isoenzymes / genetics
  • Isoenzymes / metabolism*
  • Oxidation-Reduction
  • RNA, Messenger / metabolism
  • Receptors, Estrogen / genetics
  • Receptors, Estrogen / metabolism*
  • Receptors, Retinoic Acid / genetics
  • Reference Values
  • Retinoid X Receptors
  • Transcription Factors / genetics
  • Tretinoin / pharmacology*


  • Estrogen Receptor alpha
  • Estrogen Receptor beta
  • Isoenzymes
  • RNA, Messenger
  • Receptors, Estrogen
  • Receptors, Retinoic Acid
  • Retinoid X Receptors
  • Transcription Factors
  • Tretinoin
  • 17-Hydroxysteroid Dehydrogenases