The role of miR-27a-5p in EC migration and invasion was further investigated via transfection with miR-27a-5p mimics or inhibitor in Ishikawa and HEC-1A EC cell lines.
It was found that colony stimulating factor (CSF)‑1 and CSF‑1 receptor (CSF‑1R) were highly expressed in EC tissues of patients and two EC cell lines (ECC‑1 and HEC‑1A).
The results of the present study demonstrated that miR‑409 was downregulated in human endometrial cancer, and it suppressed the growth of Ishikawa and HEC‑1B human endometrial cancer cell lines.
Not only that, silencing of PTPN18 in endometrial cancer cell lines (HEC-1-A and HEC-1-B) can significantly impair proliferation detected by CCK8 assay and flow cytometry (FCM) analyses and inhibit the metastasis of endometrial cancer cells shown by the scratch test and the Transwell experiment.
Similarly, CCAT1 was significantly upregulated in several EC cell lines (KLE, Ishiwaka and HEC-1-A), compared with the normal human endometrial stromal cell line T-HESC.
We performed an array-based lncRNA analysis of a parental HEC-50 EC cell population and derivatives with highly invasive, sphere-forming, and paclitaxel (TX)-resistant characteristics.
Here, we investigated the signaling pathway regulating the expression of HES1 and proliferation of poorly and well-differentiated endometrial cancer cell lines Ishikawa and HEC-50B, respectively.
Accordingly, the aim of the present study was to clarify whether cyclin A can be used as a cell proliferation marker using the endometrial carcinoma cell lines Ishikawa and HEC-50B, derived from patients with low-grade and high-grade cancer, respectively.
Importantly, through western blot analysis, we found that inhibition of CLDN6 remarkably decreased p-AKT, p-PI3K, and mTOR expression level in ECHEC-1B cell line.
A caspase-Glo3/7 assay was carried out to evaluate the effect of miR-423 on cisplatin-induced apoptosis in HEC-1B and Ishikawa endometrial cancer cells.
Using western blot analysis and immunofluorescence assays, it was demonstrated that overexpression of miR‑215 markedly downregulated LEFTY2 protein expression levels in HEC‑1A cells and LEFTY2 protein expression was downregulated in EC tissues, which was inversely correlated with miR‑215 expression.
We found that miR-302b-3p/302c-3p/302d-3p of the miR-302 cluster was downregulated in EC, and it altered the epithelial-mesenchymal transition (EMT) process in the EC cell lines Ishikawa and HEC-1A.
Inhibition of Expression of the S100A8 Gene Encoding the S100 Calcium-Binding Protein A8 Promotes Apoptosis by Suppressing the Phosphorylation of Protein Kinase B (Akt) in Endometrial Carcinoma and HEC-1A Cells.
RNA interference (RNAi) was used to knockdown the expression of the upregulated genes in ECC-1 and HEC-1A endometrial cancer cell lines and its effect on proliferation, migration and invasion were examined.
The mRNA and protein expression levels of ERRα and estrogen receptor α (ERα) were detected by qPCR and Western blotting in RL-952, AN3-CA, HEC-1A, and HEC-1B EC cell lines.
Last, we applied both NOTCH inhibitor DAPT and EGFR inhibitor AG1478 treatment on endometrial cancer lines IK and HEC-1A and the results suggested improvement effects of the combination therapy compared to the treatments of DAPT or AG1478 alone.
Moreover, the invasiveness, metastasis, and survival rate of HEC-1A and RL-952 endometrial cancer cells were significantly decreased (<i>P</i> < 0.001) due to the down-regulation of matriptase and HAI-1 upon increasing cisplatin concentration.