Expression of miR-200a and chemotherapeutic treatment efficacy of glioma

Abstract

The correlation between miR-200a expression and chemotherapeutic treatment efficacy of glioma was investigated. There were 45 patients with glioma in observation group whose cancer tissues, paracancerous tissues and serum samples were harvested. Additionally, there were 23 healthy subjects in the control group whose serum samples were also collected. The expression levels of miR-200a in cancer tissues, paracancerous tissues and serum samples were measured by real-time fluorescence-based quantitative polymerase chain reaction (qRT-PCR). The t-test and one-way ANOVA were used to compare the serum levels of miR-200a in patients with different clinical features involving age, sex, tumor location, pathological grade and tumor size. All patients in the observation group received temozolomide-based chemotherapy. The serum levels of miR-200a before chemotherapy were compared between patients who were responsive to chemotherapy [complete response (CR) and partial response (PR)] and patients who were not responsive to chemotherapy [stable disease (SD) and progressive disease (PD)]. The expression level of miR-200a in cancer tissue was significantly lower than that in paracancerous tissue (P<0.05). The serum level of miR-200a in patients in the observation group was lower than that in healthy subjects in the control group (P<0.05). No correlations were found between miR-200a expression and patient age, sex and tumor location (P>0.05), but miR-200a expression was found to correlate with pathological grade and tumor size (P<0.05). The expression levels of miR-200a in serum and cancer tissue in chemotherapy-non-responsive patients (SD and PD) were lower than those in chemotherapy-responsive patients (CR and PR, P<0.05). The serum levels of miR-200a in chemotherapy-responsive patients were lower than those in healthy subjects in the control group (P<0.05). Downregulation of miR-200a was associated with onset and progression of glioma, and changes of miR-200a expression levels in patients were correlated with chemotherapeutic treatment efficacy.

Circ‐U2AF1 promotes human glioma via derepressing neuro‐oncological ventral antigen 2 by sponging hsa‐miR‐7‐5p

“…Human malignant gliomas are the most common and lethal primary brain tumor in adults, and glioma cells are featured as carrying heterogeneous genetic molecular aberrations (Ben Abdallah et al, ; Cahill & Turcan, ; Fukami et al, ; Guzman, Edds, Khatua, McGovern, & Robert, ). Irrespective of the applied multimodal therapy including surgical treatment, radiotherapy, and chemotherapy, the survival of patients with glioma is exceptionally poor (Duhamel et al, ; Ju et al, ; Reitman, Winkler, & Elia, ; Scutti, ; C. Wang, Kang, Wang, Liu, & Zhao, ). Henceforth, extensive scrutiny of the molecular mechanisms beneath glioma growth may offer enhanced treatments of gliomas.…”

Long non‑coding RNA PVT1 promotes glioma cell proliferation and invasion by targeting miR‑200a

“…The miR-200 family inhibits epithelial-mesenchymal transition (EMT) by directly targeting the expression of zinc finger E-box binding homeobox 1/2 (ZEB1/ZEB2) and then inhibits the migration and invasion of tumor cells (11,12). miR-200a can inhibit the migration and invasion of cluster of differentiation 133/1+ ovarian cancer stem cells (13) and nasopharyngeal carcinoma cells (14) by downregulating ZEB2. In previous studies, miRNA arrays were used to screen miRNA expression profiles closely associated with their invasion and migration in high-grade and low-grade glioma cells (15,16).…”

The role of miR-200 family in the regulation of hallmarks of cancer

“…In contrast, miR-200a has opposite effects on drug resistance in glioma. Moreover, downregulation of miR-200a is associated with decreased chemotherapeutic treatment efficacy ( 81 ).…”