Recent researches have proved that circular RNAs (circRNAs) act as an important role in many diseases. Our study aims to uncover the role of circ-ABCB10 in the progression of non-small cell lung cancer (NSCLC).Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was utilized to detect circ-ABCB10 expression in NSCLC patients. Then, we conducted Cell Counting Kit-8 (CCK-8) assay, colony formation assay, Ethynyl deoxyuridine (EdU) incorporation assay, cell cycle assay, and cell apoptosis assay in treated NSCLC cells. Besides, further experiments including RT-qPCR and Western blot assay were performed to explore the potential mechanism in vitro.Circ-ABCB10 expression level was significantly higher in NSCLC samples comparing to that in adjacent tissues. Moreover, functional assays showed that the cell growth ability of NSCLC cells was inhibited after circ-ABCB10 was knocked down. In addition, the cell apoptosis of NSCLC cells was promoted after circ-ABCB10 was knocked down. Also the expression of KISS1 was upregulated by the knockdown of circ-ABCB10. Furthermore, it was found that KISS1 expression was negatively correlated to the circ-ABCB10 expression in NSCLC tissues.Results above indicated that circ-ABCB10 promoted cell proliferation and inhibited cell apoptosis of NSCLC by suppressing KISS1, which suggested that circ-ABCB10 may be a potential therapeutic target in NSCLC.
In the following, a short desciption for each csv files: Meta data: includes information about mice ID, scans collected from each mouse, location of extracted scans, activity of P53 gene, mouce gender, tissue type. MSpectra: contains mean spectra of tissue types with respect to each extracted scan. TissueLabels: describes different divisions of tissue types;e.g. normal vs abnormal, normal vs HB vs Karzinom, normal vs HB vs adenoma vs carcinoma Wavenumbers: includes Raman spectra wavenumbers.
<div>Abstract<p>Cancer stem cells (CSC) play a central role in cancer metastasis and development of drug resistance. miRNA are important in regulating CSC properties and are considered potential therapeutic targets. Here we report that miR-328–3p (miR-328) is significantly upregulated in ovarian CSC. High expression of miR-328 maintained CSC properties by directly targeting DNA damage binding protein 2, which has been shown previously to inhibit ovarian CSC. Reduced activity of ERK signaling in ovarian CSC, mainly due to a low level of reactive oxygen species, contributed to the enhanced expression of miR-328 and maintenance of CSC. Inhibition of miR-328 in mouse orthotopic ovarian xenografts impeded tumor growth and prevented tumor metastasis. In summary, our findings provide a novel mechanism underlying maintenance of the CSC population in ovarian cancer and suggest that targeted inhibition of miR-328 could be exploited for the eradication of CSC and aversion of tumor metastasis in ovarian cancer.</p>Significance:<p>These findings present inhibition of miR-328 as a novel strategy for efficient elimination of CSC to prevent tumor metastasis and recurrence in patients with epithelial ovarian cancer.</p></div>
Glioblastoma (GBM) patients currently face poor survival outcomes with an average survival period of less than 15 months, while only 3–5% of patients survive longer than 36 months. Although the mechanisms of tumorigenesis are still being elucidated, miRNAs are promising candidates to explore as novel and prognostic biomarkers in GBM. Here, we determined the correlation between miR-575 expression in GBM tumors and overall survival (OS) of patients and undertook functional studies to unfold the contribution of this miR to GBM tumorigenesis. Total RNAs were isolated from 268 FFPE GBM tumor samples and miR expression was assayed (simultaneously) using NanoString Technologies, and univariable and multivariable cox regression analyses were performed. Cell proliferation, colony formation, migration assay, qPCR, immunoblotting, and luciferase assay were conducted to define the function of miR-575 in GBM. Our survival analysis (n=268) show that miR-575 is associated with worse OS of GBM patients (HR=1.5, p-value=5.77E-05) by continuous UVA. miR-575 was also found to be significantly associated with OS, independent of age, gender, treatment, and KPS in a MVA (HR=1.208, p=0.012). Since miR-575 was found to be negatively associated with OS, we hypothesized that miR-575 overexpression would increase tumor progression. Our functional studies indicate that overexpression of miR-575 significantly increased the proliferation and motility of LN229 and U251 GBM cells in vitro. Consistent with the result found in LN229 and U251 cells, inhibition of miR-575 in U87 cells significantly decreased their proliferation and motility. Subsequent in silico and mechanistic studies identified p27/CDKN1B and BLID/BRCC2 aspotential target genes of miR-575 in GBM. Overexpression of miR-575 in GBM cells reduced the expression of both BLID and p27 at both mRNA and protein levels. miR-575 has prognostic value in GBM, with higher expression correlating with worse OS of patients, and contributes to GBM tumorigenesis by inhibiting expression of p27 and BLID.
'/%3e%3cuse xlink:href='%23a' transform='rotate(23.036 .093 25.536)'/%3e%3cuse xlink:href='%23a' transform='rotate(45.87 1.273 16.18)'/%3e%3cuse xlink:href='%23a' transform='rotate(69.945 .996 12.078)'/%3e%3cuse xlink:href='%23a' transform='rotate(20.66 -19.689 31.932)'/%3e%3c/svg%3e)
