LncRNA BANCR是否通过激活miR-612/CPNE3通路促进子宫内膜异位症恶变？BANCR、miR-612和CPNE3在正常子宫内膜、子宫内膜异位症在位内膜、在位子宫内膜及子宫内膜异位症相关卵巢癌恶性组织中的表达模式。以原代正常子宫内膜基质细胞（NESC）和在位子宫内膜基质细胞（EESC）为基础，在体外和体内阐明BANCR、miR-612和CPNE3之间的调控关系以及促进子宫内膜异位症恶性转化的潜在机制。 BANCR和CPNE3在正常子宫内膜中表达量最低，在位子宫内膜中表达量显着升高（P < 0.05），在位子宫内膜中表达量显着升高（P < 0.05）。子宫内膜异位症恶变过程中，BANCR、CPNE3表达水平显着上调（P < 0.05），而miR-612表达水平显着下调（P < 0.05）。 miRNA-612被发现以BANCR和CPNE3为目标。 NESC和EESC中BANCR的过表达和敲低分别上调和下调CPNE3的表达，分别促进或阻止细胞增殖和迁移；这些效应可被 miR-612 模拟物和抑制剂逆转。这些变化均具有统计学意义（P < 0.05）。体内实验显示，BANCR通过调控miR-612/CPNE3，显着提高皮下子宫内膜细胞的存活率（P < 0.05）。随着子宫内膜异位症恶变过程的进展，BANCR的表达逐渐升高，促进子宫内膜异位症的增殖和迁移。子宫内膜细胞通过 miR-612/CPNE3 途径。 BANCR 可能代表监测子宫内膜异位症恶性转化的新靶点。版权所有 © 2024 Reproductive Healthcare Ltd. 由 Elsevier Ltd 出版。保留所有权利。

Does LncRNA BANCR promote the malignant transformation of endometriosis by activating the miR-612/CPNE3 pathway?The expression patterns of BANCR, miR-612 and CPNE3 in normal endometrium, eutopic endometrium from endometriosis, eutopic endometrium or malignant tissues from endometriosis-associated ovarian cancer. On the basis of primary normal endometrial stromal cells (NESC) and eutopic endometrial stromal cells (EESC), the regulatory relationships between BANCR, miR-612 and CPNE3, and the potential mechanisms that promote the malignant transformation of endometriosis, were elucidated in vitro and in vivo.The expression levels of BANCR and CPNE3 were lowest in normal endometrium, significantly increased in eutopic endometrium (P < 0.05) and was significantly increased in eutopic endometrium (P < 0.05). During the malignant transformation of endometriosis, the expression levels of BANCR and CPNE3 were significantly upregulated (P < 0.05), whereas those of miR-612 were significantly downregulated (P < 0.05). miRNA-612 was found to target BANCR and CPNE3. The overexpression and knockdown of BANCR in NESC and EESC upregulated and downregulated the expression of CPNE3 and promoted or prevented cell proliferation and migration, respectively; these effects were reversed by miR-612 mimics and inhibitor. These changes were all statistically significant (P < 0.05). In-vivo experiments revealed that BANCR significantly increased the survival of subcutaneous endometrial cells by regulating miR-612/CPNE3 (P < 0.05).The expression of BANCR gradually increased with the progression of endometriosis during malignant transformation, and promoted the proliferation and migration of endometrial cells via the miR-612/CPNE3 pathway. BANCR may represent a novel target for monitoring the malignant transformation of endometriosis.Copyright © 2024 Reproductive Healthcare Ltd. Published by Elsevier Ltd. All rights reserved.