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Long non-coding RNA LINP1 functions as an oncogene in endometrial cancer progression by regulating the PI3K/AKT signaling pathway.

OBJECTIVE
Endometrial cancer (EC) accounts for about 6% of new cancer cases in female and about 3% of cancer-related deaths were caused by EC. The poor prognosis is mainly due to the distant spread and poor differentiation. In the current study, we want to figure out the role of long non-coding RNA (LncRNA) LINP1 in EC progression.


PATIENTS AND METHODS
The quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) assay was involved to access the expression level of LINP1 in EC cell lines and tissues. The Cell Counting Kit-8 (CCK-8) assay, colony formation assay, transwell and Matrigel assay were recruited to figure out the ability of LINP1 in cell proliferation and metastasis in EC. Subsequently, Western blotting was used to detect the expression level of PI3K/AKT in EC. Besides, we used the tumor formation assay in vivo to examine the ability of LINP1 in tumor formation in vivo.


RESULTS
LINP1 was proved to be up-regulated in EC cell lines and tissues by qRT-PCR assay. CCK-8 assay and colony formation assay were conducted and the results indicated that LINP1 over-expression can promote cell proliferation in EC in vitro. The data of transwell and Matrigel assays indicated that up-regulated LINP1 can facilitate cell migration and invasion. The results of Western blotting validated that LINP1 can activate PI3K/AKT signaling. Besides, the tumor formation assay verified that LINP1 can promote tumor formation in vivo.


CONCLUSIONS
Our research validated that LINP1 served as an oncogenic role in EC progression. The PI3K/AKT signaling pathway might be the underlying mechanism of EC progression. We hope our study can provide novel treatment targets and biomarkers in EC development and progression.