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      Placenta-Specific Protein 1: A Potential Key to Many Oncofetal-Placental OB/GYN Research Questions

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          Abstract

          Placenta-specific protein 1 (PLAC1) is a secreted protein found in trophoblasts. Several reports implicate a central role for PLAC1 in establishment and maintenance of the placenta. In addition to placentae PLAC1 is expressed in a variety of solids including breast, endometrial, and ovarian cancers. In order to show that PLAC1 is potentially relevant to a number of research questions in OB/GYN, we report on PLAC1 expression in a selected panel that includes two choriocarcinoma cell lines, normal placental tissues, and endometrial and ovarian tumors. We report for the first time that PLAC1 is also expressed in human fetal tissues. PLAC1 is transcriptionally heterogeneous with one promoter (P1) generating two transcripts with alternately spliced 5' UTRs and the other promoter (P2) generating a third transcript. Placental tissues favor P2 transcripts, while P1 is favored in most of the other cells. Mechanisms determining multiple PLAC1 transcripts and promoter preferences are as yet unknown, but it is clear that this protein is likely to be important in a variety of phenomena relevant to both gynecologic oncology and maternal-fetal medicine.

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          A placenta-specific gene ectopically activated in many human cancers is essentially involved in malignant cell processes.

          G Seitz, Özlem Türeci, Christoph Huber … (2007)
          The identification and functional characterization of tumor-specific genes is a prerequisite for the development of targeted cancer therapies. Using an integrated data mining and experimental validation approach for the discovery of new targets for antibody therapy of cancer, we identified PLAC1. PLAC1 is a placenta-specific gene with no detectable expression in any other normal human tissue. However, it is frequently aberrantly activated and highly expressed in a variety of tumor types, in particular breast cancer. RNAi-mediated silencing of PLAC1 in MCF-7 and BT-549 breast cancer cells profoundly impairs motility, migration, and invasion and induces a G1-S cell cycle block with nearly complete abrogation of proliferation. Knockdown of PLAC1 is associated with decreased expression of cyclin D1 and reduced phosphorylation of AKT kinase. Moreover, PLAC1 is localized on the surface of cancer cells and is accessible for antibodies which antagonize biological functions of this molecule. These features, in summary, make PLAC1 an attractive candidate for targeted immunotherapeutic approaches.
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            Plac1 (placenta-specific 1) is essential for normal placental and embryonic development.

            S Jackman, Xiaoyuan Kong, Michael Fant (2012)
            Plac1 is a recently identified, X-linked gene whose expression is restricted primarily to cells of the trophoblast lineage. It localizes to a chromosomal locus previously implicated in placental growth. We therefore sought to determine if Plac1 is necessary for placental and embryonic development by examining a mutant mouse model. Plac1 ablation resulted in placentomegaly and mild intrauterine growth retardation (IUGR). At E16.5, knockout (KO) and heterozygous (Het) placentae of the Plac1-null allele inherited from the mother (X(m-) X) weighed approximately 100% more than wildtype (WT) placentae, whereas the corresponding embryos weighed 7-12% less. Histologically, Plac1 mutants exhibited an expanded spongiotrophoblast layer that invaded the labyrinth. By contrast, Het placentae that inherited the null allele from the father (XX(p-) ) exhibited normal growth and were histologically indistinguishable from WT placentae, consistent with paternal imprinting of Plac1. When examined across gestation, WT and X(m-) X placental weights peaked at E16.5 and decreased slightly thereafter. KO placentae (X(m-) X(p-) and X(m-) Y), however, continued to increase in weight after E16.5, consistent with a functional role for the paternal Plac1 allele. Subsequent analysis confirmed that the paternal allele partially escapes complete X-inactivation and thus contributes to placental growth regulation. Additionally, although male Plac1 KO mice can survive, they exhibit decreased viability as a consequence of events occurring late in gestation or shortly after birth. Thus, Plac1 is a paternally imprinted, X-linked gene essential for normal placental and embryonic development. Copyright © 2012 Wiley Periodicals, Inc.
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              PLAC1, an Xq26 gene with placenta-specific expression.

              M A Cocchia, M Ko, Taylur P. Ma … (2000)
              A novel human X-linked gene shows placenta-specific expression and has been named PLAC1. The gene maps 65 kb telomeric to HPRT at Xq26 and has been completely sequenced at the cDNA and genomic levels. The mouse orthologue Plac1 maps to the syntenically equivalent region of the mouse X chromosome. In situ hybridization studies with the antisense mRNA during mouse embryogenesis detect Plac1 expression from 7.5 dpc (days postcoitum) to 14.5 dpc in ectoplacental cone, giant cells, and labyrinthine trophoblasts. The putative human and murine PLAC1 proteins are 60% identical and 77% homologous. Both include a signal peptide and a peptide sequence also found in an interaction domain of the ZP3 (zona pellucida 3) protein. These results make PLAC1 a marker for placental development, with a possible role in the establishment of the mother-fetus interface. Copyright 2000 Academic Press.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Obstet Gynecol Int
                Journal ID (iso-abbrev): Obstet Gynecol Int
                Journal ID (publisher-id): OGI
                Title: Obstetrics and Gynecology International
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 1687-9589
                ISSN (Electronic): 1687-9597
                Publication date (Print): 2014
                Publication date (Electronic): 17 March 2014
                Volume: 2014
                Electronic Location Identifier: 678984
                Affiliations
                1Department of Obstetrics and Gynecology, University of Iowa Carver College of Medicine, 3234 MERF, Iowa City, IA 52242, USA
                2Lincoln University, Lincoln University, Pennsylvania, PA 19352, USA
                3Holden Comprehensive Cancer Center, University of Iowa Hospitals and Clinics, Iowa City, IA 52242, USA
                Author notes

                Academic Editor: Robert Coleman

                Article
                DOI: 10.1155/2014/678984
                PMC ID: 3976915
                PubMed ID: 24757447
                SO-VID: 4097affd-f4f5-41a5-8a1e-864f4ab3a5f9
                Copyright © Copyright © 2014 Eric J. Devor et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 19 November 2013
                Date revision received : 23 January 2014
                Date accepted : 10 February 2014
                Funding
                Funded by: http://dx.doi.org/10.13039/100000002 National Institutes of Health
                Award ID: RO1CA99908
                Funded by: http://dx.doi.org/10.13039/100000002 National Institutes of Health
                Award ID: K12HD000849
                Funded by: http://dx.doi.org/10.13039/100000002 National Institutes of Health
                Award ID: 5K12HD063117-04
                Categories
                Subject: Research Article

                ScienceOpen disciplines: Obstetrics & Gynecology
                Data availability:
                ScienceOpen disciplines: Obstetrics & Gynecology

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