Endometriosis is a chronic disease characterized by the presence of ectopic endometrial implants [
1]. Current treatments such as medication or surgery are effective to an extent; however, some patients experience infertility, pain from ineffective treatment, recurrence, and even malignancy. Thus, identification of the mechanisms underlying the pathogenesis of endometriosis will facilitate the development of more effective treatment for this disorder.
Despite considerable investigation, the precise etiology and pathogenesis of endometriosis is unknown. To date, the leading theories are retrograde menstruation, coelomic metaplasia, embryonic cell rest, and lymphovascular metastasis [
2]. However, none of them can annotate the pathogenesis to a point for all types of endometriosis. Current research involving stem cells should shed some light on the puzzling mechanisms of this disease [
3‐
6]. However, data on stem or progenitor cell function in endometriosis are scarce due to the technical limitations to stem cell research. Current studies mainly focus on stemness-related genes; the pluripotency markers sex-determining region Y-box 2 (SOX2), Nanog homeobox (NANOG), and octamer-binding protein 4 (OCT4) are the most often studied [
7‐
9].
SOX2 is a member of the
SOX (SRY-related high mobility group [HMG] box) gene family that encodes transcription factors with a single HMG DNA-binding domain [
10].
SOX genes bind to the minor groove in DNA to control diverse developmental processes and play critical roles in cell fate determination, differentiation, and proliferation [
11]. OCT4 is a member of the POU domain transcription factor family and plays a key role in the regulation of self-renewal and pluripotency in embryonic stem cells and primordial germ cells [
12], while
NANOG is a homeobox gene and has essential roles in maintaining self-renewal and the undifferentiated state of pluripotent stem cells [
13]. In addition to maintaining the self-renewal ability of stem cells, SOX2, NANOG, and OCT4 are involved in cancer cell migration and invasion [
13‐
15]. Aberrant SOX2, NANOG, and OCT4 expression has been demonstrated in endometriotic tissues, and OCT4 promoted endometrial cell migration activity [
7‐
9]. However, these markers are not identified exclusively in women with ovarian endometriosis. Therefore, we aimed to examine and compare SOX2, NANOG, and OCT4 expression in endometrial or endometriotic tissues from women with and without ovarian endometriosis.