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The Journal of Clinical Endocrinology & Metabolism Vol. 84, No. 2 761-767
Copyright © 1999 by The Endocrine Society

Original Studies

Pituitary Tumor Transforming Gene (PTTG) Expression in Pituitary Adenomas

Xun Zhang, Gregory A. Horwitz, Anthony P. Heaney, Masahiro Nakashima, Toni R. Prezant, Marcello D. Bronstein and Shlomo Melmed

Cedars-Sinai Research Institute-University of California School of Medicine (X.Z., G.A.H., A.P.H., M. N., T.R.P., S. M.), Los Angeles, California 90048; Neuroendocrine Unit (M.D.B.), Division of Functional Neurosurgery, University of Sao Paulo Medical School, Sao Paulo, SP, Brazil

Address all correspondence and requests for reprints to: Shlomo Melmed, M.D. Academic Affairs, Room 2015, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Los Angeles, California 90048. E-mail: melmed{at}csmc.edu


   Abstract
Top
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
We recently cloned a novel pituitary tumor transforming gene (PTTG). Here we report PTTG expression in human pituitary adenomas and in normal pituitary tissue. In situ hybridization revealed PTTG expression in nonfunctioning and in GH-secreting adenomas but not in normal pituitary tissue. Using a more sensitive detection method, RT-PCR, low level PTTG expression was detected in normal pituitary. However, when expression levels in normal pituitary tissue were compared with those in 54 pituitary tumors using comparative reverse transcription polymerase chain reaction (RT-PCR), we found that most tumor samples expressed higher levels of PTTG. More than 50% PTTG increases were observed in 23 of 30 nonfunctioning pituitary tumors, all 13 GH-producing tumors, 9 of 10 prolactinomas, and 1 ACTH-secreting tumor, with more than 10-fold increases evident in some tumors. Furthermore, higher PTTG expression (P = 0.03) was observed in hormone-secreting tumors that had invaded the sphenoid bone (stages III and IV; 95% CI 3.118–9.715) compared with hormone-secreting tumors that were confined to the pituitary fossa (stages I and II; 95% CI 1.681–3.051). Therefore, PTTG abundance is a molecular marker for invasiveness in hormone-secreting pituitary tumors. The ubiquitous and prevalent expression of pituitary adenoma PTTG suggests that PTTG plays a role in pituitary tumorigenesis and invasiveness.


   Introduction
Top
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
PITUITARY tumors are common monoclonal adenomas accounting for approximately 10–15% of intracranial neoplasms. They arise from the anterior pituitary cell types (1, 2), and functioning tumors secrete pituitary trophic hormones, including prolactin (PRL), growth hormone (GH), adrenocorticotrophic hormone (ACTH), or rarely, the glycoprotein hormones LH or FSH. These hypersecretory syndromes are associated with hypogonadism, infertility, acromegaly, Cushing’s disease, or rarely, hyperthyroidism (3). Nonfunctioning (clinically silent) pituitary adenomas do not secrete detectable circulating hormones. Tumors are classified as noninvasive microadenomas (<10 mm) or macroadenomas (>10 mm). The latter may invade surrounding tissues, causing pressure symptoms and pituitary dysfunction due to stalk compression or pituitary damage (4).

The pathogenesis of pituitary tumors has been extensively studied to identify activating oncogene mutations or inactivating tumor suppressor genes (5). G protein (Gs{alpha}) mutations have been shown to be present in a subset of sporadic GH-secreting pituitary adenomas (6, 7). Rarely occurring ras mutations have been reported in invasive tumors (8, 9). Loss of heterozygosity involving chromosome 11q13 (10) or chromosome 13 (11) and loss of the purine-binding factor gene (nm23) (12) have also been linked to pituitary tumorigenesis or invasiveness. In transgenic mouse models, disruption of Rb (13) or cyclin-dependent kinase inhibitors resulted in pituitary tumor development (14, 15). However, mutations identified so far account for only a small percentage of pituitary tumors, and a more generalized mechanism for pituitary tumorigenesis remains elusive. Recently, a novel pituitary tumor transforming gene (PTTG) was isolated in our laboratory from rat GH4 pituitary tumors by differential RNA display (16). Subsequently, we cloned the human homologue of this transforming gene. Overexpression of PTTG caused in vitro cell transformation, induced in vivo tumor formation in athymic mice, and stimulated basic fibroblast growth factor (bFGF) expression and secretion (17).

We now describe human PTTG messenger RNA (mRNA) expression in pituitary adenomas determined by comparative reverse transcription-polymerase chain reaction (RT-PCR) and in situ hybridization. We demonstrate that PTTG is expressed in all pituitary tumor types, and we show that mRNA levels are higher than in normal pituitary tissue. In hormone-secreting tumors, expression of human PTTG correlates with tumor invasiveness. Therefore, enhanced PTTG expression could be an important factor involved in early pituitary tumorigenesis.


   Materials and Methods
Top
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
Patients

Fifty-four pituitary tumor specimens were obtained at surgery and immediately frozen in liquid nitrogen before analysis. The diagnosis was established by clinical, biochemical, and radiological findings and confirmed at surgery and by histology. Tumor grade and degree of invasion were determined directly at surgery as well as by pre-operative magnetic resonance imaging (MRI).

In situ hybridization

Digoxigenin-labeled RNA probes were generated by in vitro transcription using a digoxigenin RNA labeling kit (Boehringer Mannheim, Mannhein, Germany). Resected tissues were fixed in 4% paraformaldehyde overnight at 4 C. Fixed tissues were washed in 30% sucrose/0.01 M phosphate-buffered saline, embedded in octadeclyl compounds (Tissue-tek, Torrance, CA) at -80 C and sectioned (10 µm) by cryostat. After fixation, frozen tissue sections were digested with 1 µg/mL proteinase K at 37 C for 30 min, followed by post-fixation with 4% paraformaldehyde. Slides were immersed in 0.2 N HCl for 10 min and subsequently acetylated for 10 min in freshly prepared 0.25% acetic anhydride in 0.1 M triethanolamine (pH 8.0). After prehybridization in 4 x SSC/50% formamide at 37 C, slides were hybridized with antisense or sense probe in 50% deionized formamide, 10 mM Tris-HCl (pH 7.6), 1 mM EDTA (pH 8.0), 300 mM NaCl, 0.25% SDS, 1 x Denhardt’s solution, 10% dextran sulfate, and 200 µg/mL yeast tRNA at 42 C for 16 h. After hybridization, specimens were rinsed in 2 x SSC and 1 x SSC, digested with 10 µg/mL RNase A at 37 C for 30 min, and washed twice with 0.1 x SSC at 37 C for 30 min. Sections were subjected to immunohistochemistry for detection of hybridized probes using an alkaline phosphatase-conjugated antidigoxigenin antibody (Boehringer Mannheim, Indianapolis, IN). The alkaline phosphatase reaction was visualized with 5-bromo-4-chloro-3-indolyl phosphate and nitroblue tetrazolium chloride.

Comparative RT-PCR

Total RNA from human pituitary tumors and normal pituitary glands (Zoion Diagnostics, New York, NY; collected 2–5 h postmortem) were prepared using TRIZOL Reagent (Gibco BRL, Gaithersburg, MD). Tissue was homogenized in 1 mL TRIZOL Reagent and incubated at room temperature for 5 min. RNA samples were redissolved in RNase-free water for the RT-PCR reactions. Reverse transcription (RT) was performed using SuperScript Preamplification System (Gibco BRL, Gaithersburg, MD) according to the manufacturer’s protocol. Total RNA in the amount of 2.5 µg was used in each RT reaction. After reverse transcription, the samples were amplified with PCR SuperMix (Gibco BRL, Gaithersburg, MD) or PCR Master Mix (Qiagen, Valencia, CA) in the presence of {alpha}-32P-dCTP, using human PTTG-specific primers, 5'-CGATGCCCCAC-CAGCCTTACC-3' and 5'-CAAGCTCTCTCTCCTCGTCAA-GG-3', and human cyclophilin A-specific primers, 5'-CATGGTCAACCCCACCGTGTTCTT-3' and 5'-TAGATGGACTTGCCACCAGTGCCAT-3', as an internal control. Each reaction contained 0.5 µL RT product, 10 pmol of each primer, 5 µCi {alpha}-32P-dCTP, and 45 µL PCR Supermix or 95 µL PCR Master Mix. PCR reactions were carried out at 94 C, 1 min; 60 C, 1 min; 72 C, 1.5 min. PCR products were analyzed by electrophoresis in 6% sequencing gel with SequaGel System (National Diagnostics, Atlanta, GA) and exposed to BioMax-MR X-ray film (Kodak, Rochester, NY). Density of PTTG and cyclophilin A signals were recorded by scanning the film in an AlphaImager 2000 Documentation and Analysis System (Alpha Innotech Corporation, San Leandro, CA).

Statistical analysis

Each RT-PCR reaction was repeated at least five times. The relative PTTG expression level in each sample was determined by comparing PTTG and cyclophilin A signal densities and results analyzed using nonparametric t-test (Mann-Whitney Test).


   Results
Top
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
In situ tissue hybridization with antisense probes revealed PTTG expression in one nonfunctioning and one GH-secreting tumor (Fig. 1Go, a, c, and d). The PTTG signal was located in adenoma cell cytoplasm (Fig. 1Go, c and d). Hybridization signals for PTTG were not detected in normal human pituitary tissue (Fig. 1eGo), although abundant GH expression was observed as expected (Fig. 1fGo). Specificity of in situ hybridization was confirmed by absent hybridization signals when the PTTG sense probe was utilized (Fig. 1bGo).



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  		Figure 1. In situ hybridization for human PTTG in normal pituitary gland and in pituitary tumors. a, PTTG expression in a nonfunctioning adenoma (magnification x 100). b, Hybridization with PTTG sense probe in a semi-serial section of (a) (magnification x 100). c, In high power magnification (x 200), PTTG signal is detected in cell cytoplasm of a nonfunctioning adenoma. d, PTTG expression in a GH-secreting adenoma (magnification x 200). e, No PTTG expression detected in normal pituitary (magnification x 200). f, GH expression in normal pituitary (magnification x 200).

 
We previously reported PTTG mRNA expression in several pituitary tumors by Northern analysis (17). However, because most pituitary tumor specimens are extremely small, and because PTTG expression levels in normal pituitary tissue and in tumors were relatively low, it was not possible to obtain sufficient amounts of RNA from all tumor samples to perform reproducible Northern analyses. Therefore, comparative RT-PCR (18, 19) was used to assess relative PTTG expression levels in normal pituitary and in pituitary tumors. Pituitary tumors were classified according to their grades and invasive stages determined by MRI and confirmed at surgery (Table 1Go and 2Go). Total RNA was extracted from normal pituitary tissue and pituitary tumors and subjected to RT-PCR. We reasoned that when PTTG-specific primers and cyclophilin A-specific primers were used to co-amplify their respective products in the same reaction under identical conditions, the ratio of PTTG vs. cyclophilin A products would reflect the relative level of PTTG mRNA from each source. To validate this method, we performed PCR reactions with different numbers of cycles and analyzed the PCR products by densitometry. PCR primers with identical melting temperature were used to minimize differences in amplification efficiency. Results from a selected number of samples are shown in Fig 2Go. Although the PCR products generated in 25 reaction cycles were quite low, reproducible signals were always obtained in samples subjected to 30 and 35 reaction cycles. Therefore, subsequent comparisons were made using products of 30 PCR cycles, when the reaction had not yet plateaued (Fig. 2Go). Each PCR reaction was repeated at least 5 times to ensure reproducibility. A representative PCR result is shown in Fig. 3aGo. Relative PTTG expression level in each of 54 pituitary tumors and 5 normal pituitary tissue specimens was determined as the ratio of PTTG/cyclophilin A OD. Fold-increase of PTTG expression was calculated by comparing the PTTG/cyclophilin A ratio in each tumor with normal pituitary ratio when these samples were analyzed in the same PCR reactions. As shown in Fig. 3bGo, increased PTTG mRNA was present in most pituitary tumors as compared with normal pituitary tissues. Increases of more than 50% were observed in 21 of 30 nonfunctioning pituitary tumors, all 13 GH-producing tumors, 9 of 10 prolactinomas, and 1 ACTH-secreting tumor, with more than 10-fold increases evident in some tumors.


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  		Table 1. PTTG expression in 30 non-functioning pituitary tumors.

 

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  		Table 2. PTTG expression in 24 hormone secreting pituitary tumors.

 


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  		Figure 2. Measurement of PT-PCR products after different amplification cycles. PCR reactions were carried out in the presence of {alpha}-32P-dCTP and both human PTTG-specific and cyclophilin A-specific primers. After different cycles, PCR products were analyzed on a 6% sequencing gel and densitometry for each product recorded. Each PCR reaction was repeated at least three times. A representative sample from each group is shown. a, normal pituitary. b, nonfunctioning pituitary tumor. c, prolactinoma. d, somatotropinoma.

 


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  		Figure 3. Human PTTG expression in normal pituitary and pituitary tumors. a, A representative comparative RT-PCR gel. Human PTTG and cyclophilin A bands, sized 316 bp and 240 bp, respectively, are indicated. Products from reverse transcription carried out in the presence (+) and absence (-) of RT were used as template in PCR reactions. b, Ratio of PTTG vs. cyclophilin A was determined by densitometry, and fold-increase was calculated as PTTG/cyclophilin-A ratio in tumor vs. normal pituitary when the samples were analyzed in the same PCR reactions. A total of 54 pituitary tumors were analyzed, including 30 nonfunctioning tumors, 13 PRL-secreting tumors,10 GH-secreting tumors, and 1 ACTH-secreting tumor. At least 5 independent RT-PCR reactions were performed for each sample. NP, normal pituitary.

 
Clinical characteristics, tumor size, and invasiveness (Table 1Go and 2Go) were compared with respective PTTG mRNA expression levels. No correlation was found between tumor stage and PTTG mRNA level in nonfunctioning pituitary tumor samples. However, in normal-secreting tumors, significantly higher PTTG expression was observed in tumors that invaded the sphenoid bone (stage III and IV; 95% CI 3.118–9.715) (P = 0.03) compared with tumors confined to the pituitary fossa (stage I and II, 95% CI 1.681–3.051) (Fig. 4Go). Thus, in hormone-secreting tumors, PTTG expression level correlates with tumor invasiveness.



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  		Figure 4. PTTG/cyclophilin-A mRNA ratios in 24 hormone-secreting pituitary tumors. Comparison was made using t-test (Mann-Whitney Test). Tumor grade was assessed by MRI, surgical, and pathological findings.

 

   Discussion
Top
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
Using in situ hybridization, we show that human PTTG, a novel pituitary transforming gene, is expressed in pituitary adenomas but not in normal pituitary. Using RT-PCR, a much more sensitive detection method, we detected low PTTG expression in normal pituitary tissue. However, PTTG expression was higher in pituitary tumors than normal pituitary tissue, with higher expression observed in hormone-secreting tumors that invaded the sphenoid bone or expanded inferiorly into the sphenoid sinus (stages III and IV). Therefore, PTTG is the first human transforming gene to be expressed at increased levels in the majority of pituitary tumors tested. Therefore, it seems likely that PTTG plays an important role in pituitary tumorigenesis and may, in hormone-secreting tumors, be associated with invasiveness.

Several candidate genes causing pituitary tumorigenesis and tumor invasiveness have been suggested. Reduced expression of purine-binding factor nm23 was found in invasive adenomas and correlated with cavernous sinus invasion (12). Frequent loss of heterozygosity for chromosome 13q, in proximity to the retinoblastoma susceptibility gene (RB) locus was found in 13 aggressive pituitary tumors (20). As immunoreactive RB protein was detected in these tumors, another tumor suppressor gene located close to RB may be involved in preventing tumor invasion. These findings were further confirmed by identification of a chromosomal breakpoint between markers intragenic and extragenic to the RB gene on chromosome 13q (11). Loss of heterozygosity was also detected in invasive pituitary tumors and allelic deletions were found at 11q13, 13q12–14, 10q, and 1p (11). Interestingly, the chromosomal locus 11q13 harbors the MEN1 gene, a tumor suppressor gene associated with multiple endocrine neoplasia including hyperfunction or tumor formation of the parathyroids, anterior pituitary, pancreatic islets, and, rarely, carcinoid, thyroid, and adrenocortical tumors (21). However, despite 11q13 loss of heterozygosity (22, 23), theMEN1 gene appears intact in sporadic pituitary tumors not associated with MEN1 (24). Activating mutations of a G protein oncogene, Gsp, were also found in up to 40% of screened human GH-secreting adenomas (25, 26). These tumors contain constitutively active Gs{alpha} and adenylyl cyclase, and high intracellular cAMP levels (25, 7). We now report the correlation between expression of a novel oncogene, PTTG, and invasiveness in hormone-secreting pituitary tumors. Lack of an apparent correlation between PTTG expression and invasiveness in nonfunctioning pituitary tumors may suggest that different cellular mechanisms are involved in this tumor type, underscoring the heterogeneity of factors responsible for pituitary tumor invasiveness. The mechanism of tumorigenesis associated with PTTG is as yet unclear. We have shown that, in transfected cells, human PTTG stimulated bFGF expression and extracellular secretion (17). Basic fibroblast growth factor (FGF) is a potent mitogenic and angiogenic factor (27, 28) expressed in breast carcinoma (29), pancreatic carcinoma (30), and endometrial adenocarcinoma (31). In the pituitary, members of the FGF family regulate pituicyte growth, PRL transcription, and secretion (32, 33, 34). FGF-4 is also found in pituitary tumors (35, 36), where higher levels are detectable in large prolactinomas. In experimental PRL-secreting tumors, FGF-4 correlates with proliferation activity (34). Therefore, paracrine activation of growth factor expression and secretion could account for PTTG induction of pituitary tumor formation.


   Acknowledgments
 
We thank Drs. M. Weiss, H. Shahinian, and J. R. E. Davis for providing pituitary tumor specimens.

Received August 26, 1998.

Revised October 6, 1998.

Accepted October 16, 1998.


   References
Top
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

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