| BackgroundOvarian cancer ranks as the fifth leading cause of cancer-related deaths among women, and the leading cause of death from gynecological cancer. Platinum/paclitaxel-based chemotherapy is the current standard of treatment after surgical staging and resection of abdominal and pelvic cancer. The difficulty to diagnose the disease at early stage and the persistence of dormant, drug-resistant cancer cells that cause relapse, are the primary reasons for the high mortality rate in ovarian cancer patients. Therefore, it is essential to search for an effective method.Autophagy is an evolutionarily conserved catabolic process by which the cell recycles its components through self-consumption of cellular organelles and bulk cytoplasm with lysosome. It serves to keep cell homeostasis, viability, prevent chromosome abnormality disorders, sustaining genome stability. Dysregulation of autophagy has been involved in many human diseases including cancers, which has currently been a new target for investigating tumorigenesis, inhibiting tumor growth, overcoming tumor chemoresistance. Autophagy is initiated by the formation of a double-membrane bound vacuole (autophagosome), which sequesters cytosolic proteins and organelles such as mitochondria, endoplasmic reticulum. Morphologically, autophagy is characterized by the formation of LC3-â…¡ double-membrane bound autophagosomes. Microtubule-associated protein 1 light chain 3(MAPLC3), the mammalian homologue of yeast Atg8, LC3-â…¡ mainly located in the membrane of autophagosome, is involved in autophagosome formation during autophagy, specific reflection of the number of autophagy in cell body, and a specific protein marker of autophagosome.ObjectiveTo investigate the expression of microtubule-associated protein light chain 3-II(LC3-II) in the epithelial ovarian carcinoma and explore their correlations to the tumorigenesis and development of epithelial ovarian carcinoma; to elucidate the role autophagy in epithelial ovarian carcinoma development, and in order to provide some basis for intervening autophagy and offer the possibility of improved tumor control.Methods204 specimens with different-type epithelial ovarian tumors, which were confirmed by Anhui Provincial Hospital Pathology in January 2011 December 2012, including 46 with serous cystadenoma,28 with borderline serous cystadenoma,40 with serous cystadenocarcinoma,32 with mucinous cystadenoma,32 with borderline mucinous cystadenoma,28 with mucinous cystadenocarcinoma, were selected in our study. The selection of 28 cases of normal ovarian epithelial tissues was as contrast. Immunohistochemistry was employed to detect the expression of LC3-â…¡ in normal ovarian epithelial tissues and epithelial ovarian tumor tissues. The correlations between expression of LC3-II and both the pathological features and clinical manifestations of serous cystadenocarcinoma and mucinous cystadenocarcinoma patients were analyzed.Results1.LC3-II expression in ovarian tumorsLC3-II has not express in normal ovarian epithelial, The positive rates of LC3-II were significantly higher in borderline ovarian tumors and epithelial ovarian cancinoma than benign epithelial ovarian tumors. Serous cystadenoma, borderline serous cystadenoma, and serous cystadenocarcinoma, positive rate of LC3-â…¡ was 4.5%,71% and 95%(P<0.01), respectively. Mucinous cystadenoma, borderline mucinous cystadenoma, and mucinous cystadenocarcinoma, positive rate of LC3-â…¡ was 6.7%,66.7% and 92.9%(P<0.01), respectively.2.LC3-â…¡ expression relationship with clinicopathological features of ovarian cancerIn 40 cases of ovarian serous carcinoma,28 cases of ovarian mucinous carcinoma, the expression of LC3-â…¡ was not correlated to age, FIGO stage and histological grade.ConclusionsThis study investigated the expression of the key autophagy-related molecules, LC3-â…¡, in different-type epithelial ovarian tumors. We found that the expression of LC3-â…¡ is up-regulated in epithelial ovarian cancer tissues. The increase of autophagic capacity may be related to the development of epithelial ovarian cancer. |
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