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Glioblastoma Multiforme (GBM) is the most common primary malignant brain tumor. Median survival is usually less than 1 year from the time of diagnosis, and even in the most favorable situations, a majority of patients die within 2 years. Standard therapy consists of surgical resection, radiotherapy and chemotherapy. In this case report, we described a 38 y old woman with GBM survived 7 years after a series of treatments. For the patient, the tumor was found extensively infiltrate the sagittal sinus, the surgery unable completely remove of tumor, radiotherapy, chemotherapy and individualized anti-cancer herbs therapy were further applied. After all therapy, the patient was awake, with moderate bone window tension, palpable mass, right partial hemianopia, good right limb muscle strength. In summary, comprehensive treatment schedule including thorough surgical removal of tumor, systematic radiation, standard chemotherapy and individualized anti-cancer herbs therapy can help to prolong the survival of patients with GBM and gliosarcoma.

Purpose: To study miR-30b’ significance on glioblastoma, and its underlying mechanism of action. Methods: Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) while 3-(4,5)- dimethylthiahiazo (-z-y1)-3,5-di- phenytetrazoliumromide (MTT), Transwell, and xenograft tumor formation assays were carried out to study miR-30b’s effect on glioblastoma while luciferase reporter assay was employed to study the interaction between MEF2D and miR-30b. Glioblastoma cells treatment with miR-30 mimic or inhibitor were subjected to Western blot assay to study the effect of Wnt/β-catenin signaling on miR-30b/MEF2D axis-mediated cell progression. Results: MiR-30b was lowly expressed in glioblastoma tissues (p = 0.007), and this was associated with poor prognosis of patients (p = 0.022). The direct target of miR-30b was identified as MEF2D (p = 0.036). Increasing miR-30b blocked MEF2D expression in glioblastoma cells (p = 0.029). Moreover, MEF2D overturned miR-30b’ inhibitory effect on glioblastoma cell progression (p = 0.041; p = 0.006; p = 0.037). In vivo, restoration of miR-30b inhibited tumor growth (p = 0.01) and MEF2D. Interestingly, restoration of miR-30b inhibited epithelial-to-mesenchymal transition (EMT) and Wnt/β-catenin signaling pathways. Conclusion: These results indicate the critical role of miR-30b/MEF2D axis in glioblastoma via EMT and Wnt/β-catenin pathways. Thus, the miR-30b/MEF2D axis might be a beneficial therapeutic target for the management of glioblastoma patients.