Decreased Expression of HOXA10 May Activate the Autophagic Process in Ovarian Endometriosis

Autophagy is a survival process that maintains homeostasis in all eukaryotic cells. Recent studies show an abnormal autophagic activity in endometriosis, but the role of autophagy is controversial. Homeobox A10 (HOXA10) is a transcription factor necessary for embryonic and adult uterine development, and studies indicate that its expression decreases in endometriosis. Homeobox A10 may negatively regulate autophagy in endometriosis. To test this hypothesis, we measured the expression levels of autophagic biomarkers (beclin-1 and LC3-II) and HOXA10 proteins by Western blotting and messenger RNA (mRNA) by quantitative real-time polymerase chain reaction. Furthermore, we evaluated the serum cancer antigen 125 (CA125) levels by immunoassay. Most tested autophagic biomarker proteins and mRNAs were upregulated, whereas HOXA10 protein and mRNA were decreased in ovarian endometriomas compared with eutopic endometria of women with endometriosis and normal endometria. Compared with normal endometrium, only protein expression levels of autophagic biomarkers were increased in the eutopic endometrium of women with endometriosis. Moreover, HOXA10 was found to have a significant negative correlation with autophagy ( P < .01). Serum CA125 was at a high level in endometriosis and increased with elevated revised American Fertility Society staging (I-IV). There was a significant positive correlation between serum CA125 level and LC3-II protein level and/or LC3-II/LC3-I ratio ( P < .01) and a significant negative correlation between serum CA125 level and HOXA10 gene level ( P < .01). In conclusion, our studies support that the deficiency of HOXA10 may induce autophagy in endometriosis, and the relationship among CA125, autophagy, and HOXA10 in endometriosis requires additional research.