Disease relevance of XPR1

• Estrogen plays an important role in the up-regulation of Y1R, which in turn regulates estrogen-induced cell proliferation in breast cancer cells [1].
• Normal breast tissue mainly expresses the neuropeptide Y (NPY) Y2 receptor whereas primary human breast carcinomas express the Y1 receptor (Y1R) subtype [1].
• Truncated, branched, and/or cyclic neuropeptide Y (NPY) analogues were tested for their ability to bind to the neuroblastoma cells, SK-N-MC (Y1 receptor) and SK-N-BE(2) (Y2 receptor) [2].

High impact information on XPR1

• Overexpression of XPR-1 through mRNA injection increases sensitivity to progesterone and accelerates progesterone-activated cell cycle reentry [3].
• Identification of XPR-1, a progesterone receptor required for Xenopus oocyte activation [3].
• Similarly, estrogen increased Y1R mRNA expression in T-47D (ER+) but not in MDA-MB231 or MDA-MB468 (ER-) cell lines [1].
• The up-regulation of Y1R expression by estrogen is prevented by hydroxyurea but not by nocodazole or IB-MECA (cell cycle inhibitors) [1].
• Lastly, NPY inhibited estrogen-induced cell proliferation through Y1R [1].

Biological context of XPR1

• Moreover, estrogen treatment of MCF-7 cells did not increase Y1R mRNA stability [1].
• This effect is independent of increased Y1R mRNA stability or new protein synthesis, and likely occurs during S phase completion of the cell cycle [1].
• To investigate this possibility, we used estrogen receptor-positive (ER+) human breast carcinoma cell line, MCF-7, and examined the effect of estrogen on Y1R gene expression and its signaling pathways [1].
• However, it is unclear whether the mammalian orthologs of SYG-1 are also involved in local cell interactions to determine specificity during synapse formation [4].

Anatomical context of XPR1

• Finally, we show that PYY stimulates growth in Y1R-expressing gut epithelial cells that is dependent on EGFR TK activity [5].
• Treatment of female rats with estrogen in vivo decreased the levels of Y1R mRNA in the whole pituitary gland [6].
• Further, they support a role for PYY and the Y1R in regulating growth in human colonic epithelium [5].

Associations of XPR1 with chemical compounds

• Estrogen up-regulates Y1R expression through ERalpha [1].
• In conclusion, MCF-7 cells express a functional Y1R coupled to both Ca(2+) and cAMP pathways [1].
• Cycloheximide decreased basal Y1R mRNA expression; however, it did not affect its increase by estrogen [1].
• Because NPY also modulates LH release directly, we examined steroid regulation of Y1R expression in the female rat anterior pituitary [6].
• For phenobarbital tablets, a 3 X 3 X 3 factorial experiment was run [7].

Other interactions of XPR1

• Truncated, branched, and/or cyclic analogues of neuropeptide Y: importance of the pancreatic peptide fold in the design of specific Y2 receptor ligands [2].

References