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Psilopatis, I.; Pergaris, A.; , .; Tsourouflis, G.; Theocharis, S. The EPH/Ephrin System in Ovarian Cancer. Encyclopedia. Available online: https://encyclopedia.pub/entry/21322 (accessed on 05 December 2025).
Psilopatis I, Pergaris A,  , Tsourouflis G, Theocharis S. The EPH/Ephrin System in Ovarian Cancer. Encyclopedia. Available at: https://encyclopedia.pub/entry/21322. Accessed December 05, 2025.
Psilopatis, Iason, Alexandros Pergaris,  , Gerasimos Tsourouflis, Stamatios Theocharis. "The EPH/Ephrin System in Ovarian Cancer" Encyclopedia, https://encyclopedia.pub/entry/21322 (accessed December 05, 2025).
Psilopatis, I., Pergaris, A., , ., Tsourouflis, G., & Theocharis, S. (2022, April 02). The EPH/Ephrin System in Ovarian Cancer. In Encyclopedia. https://encyclopedia.pub/entry/21322
Psilopatis, Iason, et al. "The EPH/Ephrin System in Ovarian Cancer." Encyclopedia. Web. 02 April, 2022.
The EPH/Ephrin System in Ovarian Cancer
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This entry is adapted from the peer-reviewed paper 10.3390/ijms23063249

Ovarian cancer (OC) is the leading cause of death from gynecological malignancies and the fifth most common cause of tumor-related deaths in women in the United States. For 2021, the American Cancer Society estimates the incidence of OC at 21,410 cases and the OC-related deaths at 13,770 in the US. OC includes several histological types. Epithelial carcinomas comprise the vast majority of OCs, with high-grade serous OC representing the most common morphological subtype. Lack of specific symptoms of the disease at its early stages is a significant factor contributing to the typical advanced stage of the tumor at diagnosis, after metastasis has already occurred. Consequently, the 5-year survival rate for women diagnosed with invasive epithelial OC in a distant Surveillance, Epidemiology, and End Results (SEER) stage amounts to 31%. In spite of the substantial research efforts, the molecular mechanisms of OC’s origin, initiation and progression still remain largely unclear. Given the lack of effective diagnostic tools and treatment strategies, it is hence of utmost importance to identify new molecular markers involved in the pathogenesis of OC with a view to offering novel, targeted, biological therapeutic approaches.

EPHs ephrins ovarian cancer

1. The EPH/Ephrin System in OC Cell Lines and Human Xenograft Models

Many studies have investigated the role of the EPH/ephrin system in OC cell lines and human xenograft models. Cui et al., knocked down the EPHA1 gene using the CRISPR/CAS9 technique. The inactivation of EPHA1 suppressed many aggressive properties and resulted in G0/G1 cell cycle arrest, reduction of the cellular adhesion capacity, and inhibition of the migration capacity, proliferation, transwell invasion, and activity of the matrix metalloproteinase (MMP)-2 and c-MYC signaling pathways in SKOV3 and COV504 OC cells[1]. On the contrary, Jin et al., reported that EPHA1 expression was negative in HO8910 and weakly positive in A2780 OC cells, with the proliferation rate being significantly reduced in OC cells after transfection with EPHA1 plasmid compared with cells transfected with mock plasmid or untreated ones. An alteration in apoptosis could not, however, be detected in these groups[2].
EPHA2 has been described to promote the growth of OVK-18 cells[3]. Thaker et al., evaluated EPHA2 expression in OC cell lines by Western blot analysis. EG, 222, and SKOV3 OC cell lines overexpressed EPHA2, whereas A2780-PAR and HIO-180 exhibited low to absent EPHA2 expression [4]. Both OVCAR3 and SKOV3 cells demonstrated strong EPHA2 and ephrin-A1 mRNA expression, as detected through reverse transcription polymerase chain reaction (RT-PCR) and Western blot[5]. Moreover, EPHA2 overexpression promoted cell–extracellular matrix attachment in A2780 cells, increased anchorage-independent cell growth in vitro, promoted tumorigenesis in an orthotopic mouse model of OC, and resulted in enhanced microvessel density (MVD)[6].
EPHB2 demonstrated only small variations in RNA expression across OC cell lines. Promoter hypermethylation of EPHB2, EPHB3, and EPHB4 did not, however, seem to play an important role in ovarian tumors, as reported by Wu et al.[7]. Davidson et al., conducted affymetrix U133A array analysis for angiogenic gene expression in multiple OC cell lines. The genes encoding ephrin-B2 and EPHB4 were upregulated in mutant TP53 cells; ephrin-B2 was upregulated in the A2780 line; and EPHB4 was overexpressed in the larger pool of mutant TP53 lines. In contrast, EPHB2 showed high expression levels in wild-type TP53 cell lines, while overexpression of ephrin-A3 was induced by hypoxia[8]. EPHB4 was found to be highly expressed in OC cell lines and to regulate cell migration and invasion. Treatment of Hoc-7 cells with progesterone led to a dose-dependent reduction in EPHB4 expression, while inhibition of EPHB4 by specific siRNA or antisense oligonucleotides resulted in reduced viability and led to apoptosis as well as activation of the death receptor caspase pathway in this OC cell line. Interestingly, EPHB4 synthetic antisense oligodeoxynucleotides significantly inhibited tumor growth in mice-bearing human OC xenografts[9]. Ma et al., transfected antisense EPHB4 and shRNA vectors into A2780 and SKOV3 cells. Co-transfection with both vectors could inhibit growth, induce apoptosis, and reduce invasive ability of OC cells, accompanied by downregulation of EPHB4 and the PI3K/Akt/mTOR pathway[10].
Ephrin-A1 expression was shown to be induced in OC cells by the pleotropic transcription nuclear factor kappa B (NFκB) after stimulation with tumor necrosis factor alpha (TNF-α) and interleukin 1 beta (IL-1β)[11]. Ephrin-A3 expression was upregulated by hypoxia and promoted endothelial cell migration and adhesion in OC cell lines[8]. Unlike ephrin-A1, Jukonen et al., suggested that endogenous ephrin-A5 is an inefficient activator of EPHA2-pY588 signaling and receptor internalization in OC cells[12].
Ephrin-B2 was found to be overexpressed in OC cell lines[8].
Table 1 summarizes the role of the EPH/ephrin system in OC cell lines and human xenografts.
Table 1. The role of the EPH/ephrin system in OC cell lines and human xenografts.
EPHs/Ephrins Cell Lines Methods Main Results Refs.
EPHAs
EPHA1 SKOV3, COV504 RT-PCR, Western blot, cell cycle analysis, cell matrix adhesion/wound healing/invasion/ migration/motility assays Knockdown suppresses cell cycle arrest, cell adhesion migration, proliferation, and invasion. [1]
HO8910, A2780 Cell viability assay,
flow cytometry		 Low expression levels were reported only in A2780 OC cells.
Transfection with EPHA1 plasmid resulted in a significant reduction in the proliferation rate of OC cells.		 [2]
EPHA2 OVK-18 Immunoblotting, ELISA,
immunoprecipitation		 Growth promotion. [3]
HIO-180,
EG, 222, SKOV3, A2780-PAR		 Western blot, immunoprecipitation Overexpression in EG, 222, and SKOV3 OC cell lines.
Low to absent expression in A2780-PAR and HIO-180.		 [4]
OVCAR3, SKOV3 Semiquantitative RT-PCR,
Western blot		 Strong EPHA2 and ephrin-A1 mRNA expression. [5]
A2780 Western blot,
immunoprecipitation,
cell viability/attachment assay,
murine tumor xenograft model		 Increased expression resulted in the reduction of cell–cell contact, promotion of cell–extracellular matrix attachment, and an increase in anchorage-independent cell growth.
Overexpression promoted tumorigenesis, angiogenesis, and metastasis in OC xenografts.		 [6]
EPHBs
EPHB2 ES-2, OVCAR-3, OV-90, SKOV-3 Semiquantitative RT-PCR, Northern blot Similarities in RNA expression across OC cell lines and clinical samples.
No association between promoter hypermethylation of EPHB2, EPHB3, EPHB4, and OC.		 [7]
A2780wtTP53, A2780mTP53 Affymetrix U133A array analysis Upregulation in wild-type TP53 OC cell lines. [8]
EPHB4 A2780wtTP53, A2780mTP53 Affymetrix U133A array analysis Upregulation in the larger pool of mutant TP53 lines. [8]
ML5, ML10, MCV 50, HOC-7, OVCAR-3 Western blot,
cell cycle analysis, wound healing/ migration/viability/
apoptosis assays,
murine tumor xenograft model		 Upregulation in OC cell lines correlated with apoptosis inhibition, tumor cell migration and invasion.
Progesterone treatment resulted in a dose-dependent reduction in EPHB4 expression, thus promoting apoptosis via activation of the death receptor caspase pathway.
Knockdown induced apoptosis and reduced vascularization in murine OC xenografts.		 [9]
A2780,
SKOV3		 RT-PCR,
Western blot, MTT/apoptosis/migration/invasion assays		 Downregulation of EPHB4 led to cell growth inhibition, apoptosis induction, and reduced invasive ability in OC cells. [10]
Ephrins
ephrin-A1 OVCAR-3 real-time RT-qPCR,
Western blot		 NFκB induced ephrin-A1 expression after stimulation with TNF-α and IL-1β. [11]
ephrin-A3 A2780wtTP53, A2780mTP53 Affymetrix U133A array analysis Upregulation in hypoxia treated A2780mTP53 cells. [8]
ephrin-A5 OVCAR3, OVCAR4, OVCAR8 Treatment with dimeric and monomeric recombinant ephrins Endogenous ephrin-A5 inefficiently activates EPHA2–pY588 signaling and receptor internalization. [12]
ephrin-B2 A2780wtTP53, A2780mTP53 Affymetrix U133A array analysis Upregulation in the A2780mTP53 cells. [8]

2. The EPH/Ephrin System in OC Patient Tissue Samples

The upregulation of EPHA1 in OC tissues reveals its implication in disease onset and progression[13]. EPHA1 expression has been reported to be increased by more than 10-fold in OC specimens through quantitative real-time (RT-PCR)[14] and to predispose OC patients to adverse clinical outcomes[15].
Similarly, EPHA2 has led to overexpression in OC tissues in a series of studies[3][4][5][14][16]. High levels of EPHA2 protein expression have been associated with a higher tumor grade, advanced disease stage, high MVD, strong stromal reaction and epithelial matrix metalloproteinase (MMP)-9, epithelial MMP-2, and epithelial membrane-type 1 MMP expression, as well as shorter patient survival [4][5][16]. Specifically, EPHA2 processing, activated by membrane-type 1 MMP, was involved in malignant transformation of ovarian tumors[17].
EPHA4 expression in OC patients correlated with early relapse and showed an adverse clinical association when expressed in both OC tumor cells and tumor-associated macrophages[15].
On the contrary, loss of EPHA5 immunohistochemistry (IHC) expression in OC cases was shown to be associated with tumor grade, International Federation of Gynecology and Obstetrics (FIGO) stage, and poor patient outcome[18].
Liu et al., employed a tissue microarray IHC analysis and detected high EPHA8 protein expression in 44.80% of OC tissues, but only 6.67–15% of normal or benign ovarian tissues. A high EPHA8 protein level correlated with older age at diagnosis, higher FIGO stage, positive lymph nodes (LNs), the presence of metastasis, positive ascitic fluid, and higher serum CA-125 levels[19].
Loss of EPHB1 protein expression in OC tissue specimens was associated with higher tumor grade, the presence of metastasis, a high proliferative index (assessed by Ki67 expression), and significantly worse overall survival (OS)[20]. OC patients older than 60 years of age exhibited higher EPHB2 expression and poorer survival compared with younger ones[21]. On the other hand, Gao et al., performed IHC staining of EPHB3 and underlined that EPHB3 protein expression is significantly reduced in OC specimens, as well as negatively associated with histological grade and FIGO stage[22]. EPHB4 expression was shown to be upregulated in OC and correlated with an adverse clinical outcome, advanced disease stage, the presence of ascites, poorer OS, and poorer response to chemotherapy[9][15][21][23].
The expression of EPHB6 was associated with grade and TNM stage, and negatively correlated with Ki67 expression levels in OC samples, while patients with low EPHB6 protein expression exhibited a poorer outcome[24].
Elevated levels of ephrin-A1 expression led to a more aggressive tumor phenotype and were associated with poor survival in OC specimens[21]. High ephrin-A5 expression correlated with a more aggressive subtype of OC, as well as with poor patient OS[12][14][25].
High-grade OCs showed the greatest ephrin-B expression, with a strong correlation found between ephrin-B expression and MVD, disease recurrence, and a decrease in OS[26]. Schaner et al., investigated the genes that are more highly expressed in ovarian than breast carcinomas and identified ephrin-B1 as one of the best discriminators more highly expressed in OC[27]. Ephrin-B2 was overexpressed in OC tissue samples, significantly increased with clinical stages, and correlated with poor survival[23]. Ephrin-B3 has been described to correlate with EPHB4 expression in ovarian tumor specimens[28].
Table 2 summarizes the role of the EPH/ephrin system in OC tissue samples.
Table 2. The role of the EPH/ephrin system in OC tissue samples.
EPHs/Ephrins Tissue Samples Methods Main Results Refs.
EPHAs
EPHA1 8 OC samples,
8 benign ovarian samples		 IHC Upregulation in OC [13]
24 OC samples,
4 benign ovarian
samples		 real-time
RT-qPCR		 Greater than 10-fold overexpression in OC [14]
Ascites
of 28 patients with high-grade serous OC,
1 patient with serous borderline tumor		 RT-qPCR,
survival-associated gene expression analysis		 Adverse clinical association [15]
EPHA2 31 OC stroma tissue samples, 8 normal ovarian stroma samples Microarray data analysis Upregulation in the stroma of OC [3]
5 benign ovarian masses,
10 ovarian tumors of low malignant potential,
79 invasive OC samples		 IHC Overexpression in OC relates to higher tumor grade, advanced stage of disease, and significantly shorter median survival. [4]
118 advanced epithelial
OC samples		 Semiquantitative RT-PCR,
IHC		 Higher levels of protein expression correlated with a shorter disease-specific survival in OC. [5]
24 OC samples,
4 benign ovarian
samples		 real-time
RT-qPCR		 Overexpression in OC [14]
77 invasive epithelial
OC samples		 IHC Overexpression in OC is associated with increased MVD, invasion, high-grade histology, advanced FIGO stage and overexpression of stromal and epithelial MMP-9, epithelial MMP-2, and epithelial MT1-MMP. [16]
107 OC samples,
54 ovarian borderline tumors,
45 adenomas		 IHC,
Western blot,
in situ proximity ligation assay		 C-EPHA2 was expressed diffusely throughout the tumor in most OC.
In OCs, fewer signals of MT1-MMP and N-EPHA2 were observed compared with MT1-MMP and C- EPHA2.
No significant difference between MT1-MMP and C/N-EPHA2 interaction was detected in adenomas.		 [17]
EPHA4 Ascites
of 28 patients with high-grade serous OC,
1 patient with serous borderline tumor		 RT-qPCR, survival-associated gene expression analysis Adverse clinical association [15]
EPHA5 61 OC samples,
24 benign ovarian serous tumors,
42 serous borderline tumors, 20 normal fallopian tube samples		 IHC Loss of expression was associated with tumor grade, FIGO stage, and poor outcome. [18]
EPHA8 18 normal ovarian tissue samples,
20 normal fallopian tube tissue samples, 30 benign ovarian tumors, 30 borderline ovarian tumors, 125 OC samples		 RT-qPCR,
TMA-IHC		 High protein level was associated with older age at diagnosis, higher FIGO stage, positive LNs, presence of metastasis, positive ascitic fluid, and higher serum CA-125 level. [19]
EPHBs
EPHB1 74 OC samples, 12 normal ovarian epithelial tissue samples IHC Loss of expression was associated with higher tumor grade, metastasis, high proliferative index, Ki67 expression, and significantly worse OS. [20]
EPHB2 115 OC samples RT-PCR,
IHC		 OC patients older than 60 years of age exhibited higher expression than younger ones.
High levels correlated with poorer OS.		 [21]
EPHB3 19 normal fallopian tube samples, 17 serous borderline tumor samples, 50 OC specimens IHC Expression is significantly reduced in OC compared with normal fallopian tubes and borderline tumors, and is negatively associated with histological grade and FIGO stage of OC. [22]
EPHB4 7 normal ovarian specimens, 85 invasive OC samples IHC,
Western Blot		 Upregulation in invasive OC [9]
Ascites
of 28 patients with high-grade serous OC,
1 patient with serous borderline tumor		 RT-qPCR, survival-associated gene expression analysis Adverse clinical association [15]
115 OC samples RT-PCR,
IHC		 High levels correlated with poorer OS and poorer response to chemotherapy. [21]
72 OC samples Real-time
RT-PCR,
IHC		 Upregulation in OC, increased with clinical stage and correlated with poor survival. [23]
EPHB6 55 OC samples, 24 benign ovarian serous tumors, 37 serous borderline tumors, 20 normal fallopian tube samples IHC High expression was observed in 100% of normal fallopian tube samples, 100% of benign epithelial ovarian tumors, 78% of ovarian serous borderline tumors, and 18% of OC. The expression was significantly associated with grade, TNM stage, and poorer OS, and inversely associated with Ki-67. [24]
Ephrins
ephrin-A1 24 OC samples,
4 benign ovarian
samples		 real-time RT-qPCR Expression correlated with poor survival. [21]
ephrin-A5 High-grade OC samples IHC,
tissue microarrays		 Overexpression in the most aggressive high-grade OC and upregulation in the high-grade OC cells upon disease progression.
High expression was most strongly associated with poor OS.		 [12]
24 OC samples,
4 benign ovarian
samples		 real-time
RT-qPCR		 Expression correlated with poor survival. [14]
25 OC specimens, 2 normal
ovarian tissue samples, 2 benign ovarian tumors		 real-time
RT-qPCR		 Expression was associated with poorer progression-free survival. [25]
ephrin-B 112 OC samples IHC,
Western blot		 High-grade OC showed greatest expression.
A correlation was found between ephrin-B expression and MVD.
Expression was associated with higher rates of disease recurrence and a decrease in OS.		 [26]
ephrin-B1 162 OC samples IHC Upregulation in OC cell lines. [27]
ephrin-B2 72 OC samples Real-time
RT-PCR,
IHC		 Upregulation in OC, increase with clinical stage, and correlation with poor survival. [23]

References

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Subjects: Obstetrics & Gynaecology
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