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Overexpression of miR-200s in murine ovarian cancer cells (ID8 and 28-2)

ABSTRACT: Little is known about the role of miR-200s in the progression of ovarian cancer. In this study we overexpressed the miR-200c/141 cluster, the miR-200b/200a/429 cluster, or both clusters in two different murine ovarian cancer cell lines (ID8 and 28-2). As co-oeverexpression of both clusters provided the best miR-200 overexpression, we evaluated ID8 and 28-2 cells overexpressing both miR-200 clusters (ID8-200f and 28-2-200f) compared to empty vector control cells (ID8EV and 28-2EV). ID8-200f and 28-2-200f cells showed increased expression of several mesenchymal genes, decreased proliferation, decreased invasion and increased apoptosis compared to their respective controls. RNA sequencing of ID8EV, ID8-200f, 28-2EV and 28-2-200f cells revealed that overexpression of miR-200s primary regulated genes involved in epithelial mesenchymal transition EMT) and gene implicated in migration. Therefore, our work suggests that miR-200s can inhibit characteristics associated ovarian cancer progression (increased proliferation and invasion and promotion of EMT).

ORGANISM(S): Mus musculus

PROVIDER: GSE250195 | GEO | 2024/07/03

REPOSITORIES: GEO

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Project description:Epithelial-mesenchymal transition (EMT) has recently been recognized as a key element of cell invasion, migration, metastasis, and drug resistance in several types of cancer, including non-small cell lung cancer (NSCLC). Our aim was to clarify microRNA (miRNA) -related mechanisms underlying EMT followed by acquired resistance to epidermal growth factor receptor tyrosine-kinase inhibitor (EGFR-TKI) in NSCLC. MiRNA expression profiles were examined before and after transforming growth factor-beta1 (TGF-M-NM-21) exposure in four human adenocarcinoma cell lines with or without EMT. Correlation between expressions of EMT-related miRNAs and resistance to EGFR-TKI gefitinib was evaluated. MiRNA array and quantitative RT-PCR revealed that TGF-M-NM-21 significantly induced overexpression of miR-134, miR-487b, and miR-655, which belong to the same cluster located on chromosome 14q32, in lung adenocarcinoma cells with EMT. MAGI2 (membrane-associated guanylate kinase, WW and PDZ domain-containing protein 2), a predicted target of these miRNAs and a scaffold protein required for PTEN (phosphatase and tensin homolog), was diminished in A549 cells with EMT after the TGF-M-NM-21 stimulation. Overexpression of miR-134 and miR-487b promoted the EMT phenomenon and affected the drug resistance to gefitinib, whereas knockdown of these miRNAs inhibited the EMT process and reversed TGF-M-NM-21-induced resistance to gefitinib. Our study demonstrated that the miR-134/487b/655 cluster contributed to the TGF-M-NM-21-induced EMT phenomenon and affected the resistance to gefitinib by directly targeting MAGI2, whose suppression subsequently caused loss of PTEN stability in lung cancer cells. The miR-134/miR-487b/miR-655 cluster may be new therapeutic targets in advanced lung adenocarcinoma patients, depending on the EMT phenomenon. miRNA expression profiles before and after TGF-M-NM-21 exposure were assessed in the four lung adenocarcinoma cell lines, A549, LC2/ad, PC3, and, PC9 by TaqMan miRNA arrays. Relative ratios of miRNAs in cells after TGF-M-NM-21 exposure were calculated when compared with the cells before TGF-M-NM-21 exposure.

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Overexpression of miR-200s in murine ovarian cancer cells (ID8 and 28-2)

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