Knocking down of LINC01220 inhibits proliferation and induces apoptosis of endometrial carcinoma through silencing MAPK11

Abstract

Background: Endometrial carcinoma (EC) still threatens the health of women. Thus, to explore how long intergenic non-protein coding RNA 01220 regulates the development of EC. Methods: Whole genome expression profile data of EC and paracancerous tissues in TCGA database were downloaded. LINC01220 expression in EC and paracancerous tissues of patients in our hospital were detected by qRT-PCR. Furthermore, the relationship between LINC01220 expression and clinicopathological features of EC patients was analyzed. After transfection with sh-LINC01220 and pcDNA-MAPK11 (mitogen-activated protein kinase) in EC cells, proliferative, colony formation abilities and apoptosis were determined by cell counting kit-8 (CCK-8), colony formation assay and flow cytometry, respectively. Western blot was conducted to determine the regulatory role of LINC01220 on MAPK11. Results: TCGA data showed that LINC01220 expression is markedly higher in EC tissues than that of paracancerous tissues, which was consistent without detection in EC patients of our hospital. LINC01220 expression was positively correlated to pathological grade and International Federation of Gynecology and Obstetrics (FIGO) stage of EC patients. After knockdown of LINC01220 in EC cells, proliferative and colony formation abilities decreased, whereas apoptotic rate increased. Cor function analysis revealed the positive correlation between LINC01220 and MAPK11 in EC. MAPK11 expression was regulated by LINC01220 in EC cells. Overexpression of MAPK11 can reverse the tumor suppressing effect of LINC01220 on EC. Conclusions: LINC01220 promotes EC development by stimulating proliferation and inhibiting apoptosis of EC cells through up-regulating MAPK11.

<p>Silencing of Long Non-Coding RNA LINC01106 Suppresses the Proliferation, Migration and Invasion of Endometrial Cancer Cells Through Regulating the miR-449a/MET Axis</p>

“…11 LINC01220 expression is dramatically up-regulated in EC tissues and its high expression is strongly associated with tumor stage. 30 Consistent with the above two findings, we revealed that the expression of LINC01106 was obviously elevated in EC tissues and cells, and high expression of LINC01106 presented a notable connection with the tumor stage. In addition, we also demonstrated that LINC01106 was correlated with tumor metastasis.…”

“…2,3 Many lncRNAs are taken part in the occurrence of EC. 11,30 LINC01410 is highly expressed both in EC tissues and cells and the up-regulation of LINC01410 is closely related to tumor stage. 11 LINC01220 expression is dramatically up-regulated in EC tissues and its high expression is strongly associated with tumor stage.…”

“…Also, some lncRNAs have been found to act as important regulators in cell proliferation, migration and invasion and apoptosis in EC. 10,14,30 For instance, LINC01220…”

“…Gao et al silencing suppresses the proliferation and facilitates the apoptosis of EC cells. 30 The proliferation and invasion of EC cells are restrained by LINC01410 knockdown. 11 Suppression of LINC01016 inhibits the proliferation, migration and invasion of EC cells.…”

p38β and Cancer: The Beginning of the Road

“…In endometrial cancer, p38β has been shown to mediate the proliferation of tumor cells by inhibiting apoptosis. In this case, the anti-apoptotic ability of p38β seems to be controlled by the long non-coding RNA 1220, that controls p38β expression [ 90 ]. Interestingly, in lung cancer it has been recently reported that p38α, but not the rest of p38MAPK members, could be a potential biomarker of chemotherapy response [ 68 ].…”