Background: Autophagy exists widely in various physiological and pathological conditions.
Lots of investigations have verified that the autophagic activity is always related to the occurrence
and the development of cancer. Endometriosis (EMs) is a disease that endometrium-like tissues
abnormally grow outside the uterus and also considered to possess the characters of tumor because of
its malignant biological behavior.
Introduction: Recently, several studies have already revealed that autophagy may play a potential role
in proliferative-phase EMs. However, the function of autophagic activity in secretory-phase EMs is
Methods: In our work, we explored autophagic activity between normal endometrium and EMs lesion
endometrium during different menstrual phases and EMs stages. The clinical endometrium samples
from 73 women were selected in this study, including 30 healthy individuals and 43 patients with EMs
(endometrium samples include eutopic and its matched ectopic endometrium). All the participants
were divided into two groups according to the menstrual cycle, namely proliferative-phase and secretive-
phase group. Among the patients with EMs, 22 individuals in proliferative phase and the other 21
individuals in secretory phase were further classified into the groups of Stage I-II and Stage III-IV according
to revised-American Fertility Society (r-AFS). Two autophagy-related proteins microtubuleassociated
protein 1 light chain 3 beta-II (LC3B-II) and sequestosome protein (P62), which are believed
to be the indicators of autophagy activity, were chosen in the study. Immunohistochemical
(IHC) staining, Western blot assay and Real-Time quantitative Polymerase Chain Reaction (RTqPCR)
were used to examine the expression of LC3B-II and P62 in protein and mRNA level
Result: It showed that the expression of LC3B-II both in protein and mRNA level decreased and that
of P62 increased in secretory phase of the healthy group (P<0.05), but showed no significant difference
in ectopic and its eutopic endometrium group during proliferative and secretory phase (P>0.05).
In addition, the expression of LC3B-II in ectopic endometrium group was significantly lower than that
of its eutopic endometrium group (P<0.05), and the expression of P62 was significantly higher accordingly
(P<0.05). At the same time, both LC3B-II and P62 levels remained same between eutopic endometrium
group and control group (P>0.05). Furthermore, compared to Stage I-II EMs group, the
expression of LC3B-II was significantly lower (P<0.05) and P62 was significantly higher (P<0.05) in
Stage III-IV EMs during secretory phase.
Conclusion: Taken together, the periodicity-losing in EMs and the decreased autophagic activity in
ectopic endometrium may exert a potential role in the pathogenesis of EMs. Down-regulated autophagy
of ectopic endometrium in secretory phase may be related to the progression of EMs.