Prolactin Stimulates Mitogen-Activated Protein Kinase in Human Leiomyoma Cells

Nohara, A.; Ohmichi, Masahide; Koike, Koji; Jikihara, Hiroaki; Kimura, Akiko; Masuhara, Kensaku; Ikegami, Hiromasa; Inoue, Masakí; Miyake, Akira; Murata, Yuji

doi:10.1006/bbrc.1997.7322

Cited by 23 publications

(12 citation statements)

References 35 publications

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“…On the other hand, there was no significant difference between the groups in the proportion of women who had had a cumulative lactation period over 9 months with the values falling in relatively close range (32.9 vs. 42.24%; table 2). Overall, these findings support the previous hypothesis stating that prolactin, the most prominent hormone during lactation, may increase the risk for development of fibroid tumors [23]. …”

Section: Discussionsupporting

confidence: 91%

Gene Expression Patterns of Insulin-Like Growth Factor 2 in Human Uterine Fibroid Tissues: A Genetic Study with Clinical Correlations

Csatlós¹,

Rigó²,

Laky³

et al. 2013

Gynecol Obstet Invest

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Background/Aims: We investigated insulin-like growth factor 2 (IGF-2) gene activity in human uterine fibroid tissue. Results of the genetic testing were correlated with clinical data. Methods: We obtained samples from patients treated for uterine fibroid and from patients undergoing hysterectomy due to other indications (control group). The examined group (with fibroid) contained 101 cases, while the control group was similar with 110 patients. Gene expression values were determined using the standard PCR technique. Clinical data were available from the computer database of the department. Results: IGF-2 gene expression was significantly higher in the fibroid group. There was no correlation between increase in gene activity and the number of tumors. History of previous uterine fibroid did not seem to predict IGF-2 gene activity in the current fibroid tumor tissue. IGF-2 gene expression did not correlate with cumulative duration of lactation following prior pregnancies. Conclusion: IGF-2 gene activity is significantly increased in leiomyoma tissue compared to normal myometrium. Familial aggregation of uterine fibroids is not significantly associated with increased IGF-2 gene activity; other genes may have a stronger etiological role. It appears that the genetic factors potentially important in the development of familiar uterine leiomyoma are not related to the IGF-2 gene.

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Section: Discussionsupporting

confidence: 91%

Gene Expression Patterns of Insulin-Like Growth Factor 2 in Human Uterine Fibroid Tissues: A Genetic Study with Clinical Correlations

Csatlós¹,

Rigó²,

Laky³

et al. 2013

Gynecol Obstet Invest

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“…The diverse activities of PRL are mediated by its receptor (PRLR) and this molecule evokes the activation of several signaling pathways including Jak2-STAT [3], PI3K [4], and MAPK [5,6]. There are multiple isoforms of the PRLR in humans; the long form (LF), intermediate (IF), and two short forms (SF1a and SF1b) are produced by alternative splicing [7].…”

Section: Introductionmentioning

confidence: 99%

Prolactin and Prolactin Receptor Expression in Cervical Intraepithelial Neoplasia and Cancer

Ascencio-Cedillo

López-Pulido

Muñoz‐Valle

et al. 2014

Pathol. Oncol. Res.

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Prolactin receptor (PRLR) overexpression could play a role in tumorigenesis. The aim of this study was to determine prolactin (PRL) and PRLR expression in biopsies from patients with precursor lesions and uterine cervical cancer. PRLR expression was analyzed in 63 paraffin-embedded biopsies of uterine cervical tissue. In total, eleven low-grade squamous intraepithelial lesions (LSIL), 23 high-grade squamous intraepithelial lesions (HSIL), 21 uterine cervical cancers (UCC) and 8 normal epithelium (NE) were examined using immunoperoxidase staining and Western blot analysis. Additionally, PRL expression was identified in human cervical cancer serum and tissues. The PRLR expression was found to be significantly increased in cervical cancer in comparison with normal tissue and precursor lesions (P < 0.0003). The presence of the long isoform of the PRLR was observed only in cervical cancer tissues. Serum PRL levels were normal in all samples and local prolactin expression was similar in precursor lesions and cervical cancer by Western blot analysis. Our data suggest a possible role for PRLR in the progression of cervical cancer.

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“…The putative genomic signaling pathways of PRL in mammary glandular epithelia, neurons and liver appeared to involve Janus kinase-2 (JAK2) signal transducers and activator of transcription (STAT)5, phosphoinositide 3-kinase (PI3K), and mitogen-activated protein kinase/extracellular signal-regulated kinase (MEK) pathways (6,30,42,55,62). However, nongenomic cascades of JAK2, PI3K, and MEK have also been demonstrated as sig-naling pathways of PRL in several tissues, including mammary epithelia (1,47,51).…”

mentioning

confidence: 99%

Prolactin-stimulated transepithelial calcium transport in duodenum and Caco-2 monolayer are mediated by the phosphoinositide 3-kinase pathway

Jantarajit¹,

Thongon²,

Pandaranandaka³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

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Jantarajit W, Thongon N, Pandaranandaka J, Teerapornpuntakit J, Krishnamra N, Charoenphandhu N. Prolactin-stimulated transepithelial calcium transport in duodenum and Caco-2 monolayer are mediated by the phosphoinositide 3-kinase pathway. Am J Physiol Endocrinol Metab 293: E372-E384, 2007. First published May 8, 2007; doi:10.1152/ajpendo.00142.2007 has been shown to stimulate intestinal calcium absorption but the mechanism was still unknown. This study aimed to investigate the mechanism and signaling pathway by which PRL enhanced calcium transport in the rat duodenum and Caco-2 monolayer. Both epithelia strongly expressed mRNAs and proteins of PRL receptors. Ussing chamber technique showed that the duodenal active calcium fluxes were increased by PRL in a dose-response manner with the maximal effective dose of 800 ng/ml. This response diminished after exposure to LY-294002, a phosphoinositide 3-kinase (PI3K) inhibitor. Caco-2 monolayer gave similar response to PRL with the maximal effective dose of 600 ng/ml. By nullifying the transepithelial potential difference, we showed that the voltage-dependent paracellular calcium transport did not contribute to the PRL-enhanced flux in Caco-2 monolayer. In contrast, the calcium gradient-dependent paracellular transport and calcium permeability were increased by PRL. Effects of PRL on Caco-2 monolayer were abolished by PI3K inhibitors (LY-294002 and wortmannin), but not by inhibitors of MEK (U-0126) or JAK2 (AG-490). To investigate whether the PRL-enhanced paracellular transport was linked to changes in the epithelial charge selectivity, the permeability ratio of sodium and chloride (P Na/PCl) was determined. We found that PRL elevated the P Na/PCl in both epithelia, and the effects were blocked by PI3K inhibitors. In conclusion, PRL directly and rapidly stimulated the active and passive calcium transport in the rat duodenum and Caco-2 monolayer via the nongenomic PI3K-signaling pathway. This PRL-enhanced paracellular calcium transport could have resulted from altered charge selectivity. charge selectivity; dilution potential; paracellular transport; prolactin receptor; tight junction; transcellular transport AS ONE OF THE CALCIUM-REGULATING HORMONES during pregnancy and lactation, prolactin (PRL) has been shown to stimulate intestinal calcium absorption (38), thereby protecting against development of negative calcium balance during these reproductive periods. Further investigations in nonmated female rats also revealed stimulatory actions of PRL on intestinal calcium absorption (11, 54), especially in the duodenum which was the most efficient site for calcium transport (21,32). Although the presence of PRL receptor (PRLR) proteins in duodenal enterocytes of rats was controversial, expression of rat PRLR (rPRLR) transcripts in the duodenal mucosa, demonstrated by in situ hybridization technique (45), implicated a direct action of PRL on the duodenal epithelial cells.Calcium traversed the duodenal epithelium by both active and passive pathways with the former being neglig...

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Prolactin Stimulates Mitogen-Activated Protein Kinase in Human Leiomyoma Cells

Cited by 23 publications

References 35 publications

Gene Expression Patterns of Insulin-Like Growth Factor 2 in Human Uterine Fibroid Tissues: A Genetic Study with Clinical Correlations

Gene Expression Patterns of Insulin-Like Growth Factor 2 in Human Uterine Fibroid Tissues: A Genetic Study with Clinical Correlations

Prolactin and Prolactin Receptor Expression in Cervical Intraepithelial Neoplasia and Cancer

Prolactin-stimulated transepithelial calcium transport in duodenum and Caco-2 monolayer are mediated by the phosphoinositide 3-kinase pathway

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