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1.邯郸市中心医院妇一科,河北 邯郸 056000
2.邯郸市中心医院产一科,河北 邯郸 056000
马建彩,E-mail:majiancai68@163.com
纸质出版日期:2025-01-25,
收稿日期:2024-03-07,
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石媛媛, 田芬, 周玮月, 等. LINC00839对子宫内膜癌细胞恶性生物学行为的影响及机制[J]. 局解手术学杂志, 2025,34(1):21-27.
SHI YUAN-YUAN, TIAN FEN, ZHOU WEI-YUE, et al. Effect and mechanism of LINC00839 on the malignant biological behavior of endometrial cancer cells. [J]. Journal of regional anatomy and operative surgery, 2025, 34(1): 21-27.
石媛媛, 田芬, 周玮月, 等. LINC00839对子宫内膜癌细胞恶性生物学行为的影响及机制[J]. 局解手术学杂志, 2025,34(1):21-27. DOI: 10.11659/jjssx.03E024035.
SHI YUAN-YUAN, TIAN FEN, ZHOU WEI-YUE, et al. Effect and mechanism of LINC00839 on the malignant biological behavior of endometrial cancer cells. [J]. Journal of regional anatomy and operative surgery, 2025, 34(1): 21-27. DOI: 10.11659/jjssx.03E024035.
目的
2
探究LINC00839调节miR-625-5p/胞质多聚腺苷酸化元件结合蛋白4(CPEB4)轴对子宫内膜癌细胞恶性生物学行为的影响。
方法
2
获取46例子宫内膜癌患者的癌组织及癌旁组织,体外培养子宫内膜癌细胞HEC-1B、Ishikawa、RL95-2及人子宫内膜上皮细胞(HEEC),检测组织和细胞中LINC00839、miR-625-5p和CPEB4表达水平。将HEC-1B细胞分为HEC-1B组(常规培养)、sh-Ctrl组(转染sh-Ctrl)、sh-LINC00839组(转染shRNA-LINC00839)、anti-miR-625-5p组(转染shRNA-LINC00839和miR-625-5p抑制物)、anti-NC组(转染shRNA-LINC00839和inhibitor-NC)。比较各组HEC-1B细胞增殖、凋亡、迁移和侵袭能力,并测定CPEB4和上皮-间质转化(EMT)相关蛋白表达。分析LINC00839与miR-625-5p、miR-625-5p与CPEB4的靶向关系。
结果
2
子宫内膜癌组织中LINC00839、CPEB4的mRNA表达和CPEB4蛋白阳性表达率高于癌旁组织(
P
<
0.05),miR-625-5p表达低于癌
旁组织(
P
<
0.05)。与HEEC细胞相比,Ishikawa、RL95-2和HEC-1B细胞中LINC00839、CPEB4 mRNA和蛋白表达升高(
P
<
0.05),miR-625-5p表达降低(
P
<
0.05)。与sh-LINC00839组、anti-NC组比较,HEC-1B组、sh-Ctrl组、anti-miR-625-5p组HEC-1B细胞的N-钙黏蛋白(N-cadherin)、波形蛋白(Vimentin)、CPEB4蛋白表达和24 h吸光度、迁移和侵袭细胞数升高/增加(
P
<
0.05),E-钙黏蛋白(E-cadherin)蛋白表达和细胞凋亡率降低(
P
<
0.05)。LINC00839和miR-625-5p、miR-625-5p和CPEB4之间存在结合位点,具有靶向调控关系。
结论
2
LINC00839与子宫内膜癌细胞恶性生物学行为有关,干扰LINC00839表达可抑制HEC-1B细胞增殖、侵袭与迁移,促进凋亡,其作用机制可能是通过调控miR-625-5p/CPEB4轴实现。
Objective
2
To investigate the effect of LINC00839 on the malignant biological behavior of endometrial cancer cells by regulating the miR-625-5p/cytoplasmic polyadenylation element binding protein 4 (CPEB4) axis.
Methods
2
The cancer tissues and adjacent tissues of 46 patients with endometrial cancer were obtained, endometrial cancer cells of HEC-1B, Ishikawa and RL95-2 and human endometrial epithelial cells (HEEC) were cultured in vitro, and the expression levels of LINC00839, miR-625-5p and CPEB4 in tissues and cells were detected. HEC-1B cells were divided into the HEC-1B group (conventional culture), sh-Ctrl group (transfected with sh-Ctrl), sh-LINC00839 group (transfected with shRNA-LINC00839), anti-miR-625-5p group (transfected with shRNA-LINC00839 and miR-625-5p inhibitor), and anti-NC group (transfected with shRNA-LINC00839 and inhibitor-NC). The proliferation, apoptosis, migration and invasion abilities of HEC-1B cells in each group were compared, and the expressions of CPEB4 and epithelial-mesenchymal transition (EMT) related proteins were determined. The targeting relationships between LINC00839 and miR-625-5p, and miR-625-5p and CPEB4 were analyzed.
Results
2
The mRNA expression of LINC00839 and CPEB4, as well as the positive expression rate of CPEB4 protein in endometrial cancer tissu
es were higher than those in adjacent tissues, and the expression of miR-625-5p was lower than that in adjacent tissues (
P
<
0.05). Compared with HEEC cells, the expression of LINC00839 and the mRNA and protein expression of CPEB4 in Ishikawa, RL95-2 and HEC-1B cells increased (
P
<
0.05), and the expression of miR-625-5p decreased (
P
<
0.05). Compared with the sh-LINC00839 group and anti-NC group, the protein expression of N-cadherin, Vimentin, and CPEB4, 24-hour absorbance, and migration and invasion cell numbers of HEC-1B cells in the HEC-1B group, sh-Ctrl group and anti-miR-625-5p group increased (
P
<
0.05), while the expression of E-cadherin protein and cell apoptosis rate decreased (
P
<
0.05). There were binding sites between LINC00839 and miR-625-5p, miR-625-5p and CPEB4, with targeting regulatory relationships.
Conclusion
2
LINC00839 is related to the malignant biological behavior of endometrial cancer cells, interference with LINC00839 expression can inhibit the proliferation, invasion and migration,and promote apoptosis of HEC-1B cells, and its mechanism may be achieved by regulating the miR-625-5p/CPEB4 axis.
LINC00839miR-625-5p/CPEB4轴子宫内膜癌恶性生物学行为
LINC00839miR-625-5p/CPEB4 axisendometrial cancermalignant biological behavior
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