Glioma, which accounts for more than 30% of primary central nervous system tumours, is characterised by symptoms such as headaches, epilepsy, and blurred vision. Glioblastoma multiforme is the most aggressive, malignant, and lethal brain tumour in adults. Even with progressive combination treatment with surgery, radiotherapy, and chemotherapy, the prognosis for glioma patients is still extremely poor. Compared with the poor outcome and slowly developing technologies for surgery and radiotherapy, the application of targeted chemotherapy with a new mechanism has become a research focus in this field. Moreover, targeted therapy is promising for most solid tumours. The tumour-tropic ability of stem cells, including neural stem cells and mesenchymal stem cells, provides an alternative therapeutic approach. Thus, mesenchymal stem cell-based therapy is based on a tumour-selective capacity and has been thought to be an effective anti-tumour option over the past decades. An increasing number of basic studies on mesenchymal stem cell-based therapy for gliomas has yielded complex outcomes. In this review, we summarise the biological characteristics of human mesenchymal stem cells, and the current status and potential challenges of mesenchymal stem cell-based therapy in patients with malignant gliomas.

Tumor‐associated macrophage (TAM) infiltration facilitates glioma malignancy, but the underlying mechanisms remain unclear. Herein, it is reported that TAMs secrete exosomal LINC01232 to induce tumor immune escape. Mechanistically, LINC01232 is found to directly bind E2F2 and promote E2F2 entry into the nucleus; the two synergistically promots the transcription of NBR1. The increase in binding between NBR1 binding and the ubiquitinating MHC‐I protein through the ubiquitin domain causes an increase in the degradation of MHC‐I in autophagolysosomes and a decrease in the expression of MHC‐I on the surface of tumor cells, which in turn led to tumor cell escape from CD8⁺ CTL immune attack. Disruption of E2F2/NBR1/MHC‐I signaling with shRNAs or blockade with the corresponding antibodies largely abolishes the tumor‐supportive effects of LINC01232 and inhibits tumor growth driven by M2‐type macrophages. Importantly, knockdown of LINC01232 enhances the expression of MHC‐I on the surface of tumor cells and improves the response to reinfusion with CD8⁺ T cells. This study reveals the existence of critical molecular crosstalk between TAMs and glioma mediates through the LINC01232/E2F2/NBR1/MHC‐I axis to support malignant tumor growth, indicating that targeting this axis may have therapeutic potential.

Improving the chemotherapy resistance of temozolomide (TMZ) is of great significance in the treatment of glioblastoma multiforme (GBM). Long non‐coding RNA just proximal to the X‐inactive specific transcript (JPX) has been proven to be involved in cancer progression. However, the intrinsic significance and molecular mechanism by which JPX orchestrates GBM progression and TMZ chemotherapy resistance remain poorly understood. Here, JPX was found to be significantly elevated in GBM tissues and cell lines, and patients with high expressions of JPX showed significantly worse prognoses. Functional experiments revealed its carcinogenic roles in GBM cell proliferation, TMZ chemoresistance, anti‐apoptosis, DNA damage repair, and aerobic glycolysis. Mechanistically, JPX formed a complex with phosphoinositide dependent kinase‐1 (PDK1) messenger RNA (mRNA) and promoted its stability and expression. Furthermore, an RNA immunoprecipitation (RIP) experiment showed that JPX interacted with N6‐methyladenosine (m6A) demethylase FTO alpha‐ketoglutarate dependent dioxygenase (FTO) and enhanced FTO‐mediated PDK1 mRNA demethylation. JPX exerted its GBM‐promotion effects through the FTO/PDK1 axis. Taken together, these findings reveal the key role of JPX in promoting GBM aerobic glycolysis and TMZ chemoresistance in an m6A‐dependent manner. Thus, it comprises a promising novel therapeutic target for GBM chemotherapy.

Background: Ferroptosis has been linked to tumor progression and resistance to antineoplastic therapy. Long noncoding RNA (lncRNA) exerts a regulatory role in various biological processes of tumor cells, while the function and molecular mechanism of lncRNA in ferroptosis are yet to be clarified in glioma. Methods: Both gain-of-function and loss-of-function experiments were employed to investigate the effects of SNAI3-AS1 on the tumorigenesis and ferroptosis susceptibility of glioma in vitro and in vivo. Bioinformatics analysis, Bisulfite sequencing PCR, RNA pull-down, RIP, MeRIP and dual-luciferase reporter assay were performed to explore the low expression mechanism of SNAI3-AS1 and the downstream mechanism of SNAI3-AS1 in ferroptosis susceptibility of glioma. Results: We found that ferroptosis inducer erastin downregulates SNAI3-AS1 expression in glioma by increasing the DNA methylation level of SNAI3-AS1 promoter. SNAI3-AS1 functions as a tumor suppressor in glioma. Importantly, SNAI3-AS1 enhances the anti-tumor activity of erastin by promoting ferroptosis both in vitro and in vivo. Mechanistically, SNAI3-AS1 competitively binds to SND1 and perturbs the m⁶A-dependent recognition of Nrf2 mRNA 3’UTR by SND1, thereby reducing the mRNA stability of Nrf2. Rescue experiments confirmed that SND1 overexpression and silence can rescue the gain- and loss-of-function ferroptotic phenotypes of SNAI3-AS1, respectively. Conclusions: Our findings elucidate the effect and detailed mechanism of SNAI3-AS1/SND1/Nrf2 signalling axis in ferroptosis, and provide a theoretical support for inducing ferroptosis to improve glioma treatment.

Purpose This paper examines the application of 3D printing technology in the endoscopic endonasal approach for the treatment of macroadenomas. Methods We have retrospectively analysed 20 patients who diagnosed with macroadenoma underwent endoscopic transsphenoidal surgery in Wuhan Union hospital from January 2017 to May 2017. Among the 20 patients, 10 patients received the service of 3D printing technology preoperatively. The data of 3D processing and clinical result were recorded for further evaluation. Results The 10 patients who received the service had a successful 3D printed model of their tumors, it shows the anatomy of sphenoid sinus, tumor location which were in good agreement with our intraoperative observations. The 10 patients who received the service had a less operation time (127.0 ± 15.53 vs. 143.40 ± 17.89), blood loss (159.90 ± 12.31 vs. 170.00 ± 29.06) and less postoperative complication rate (20% vs. 40%). the design time of the 3D images varies 2 h 10 min to 4 h 32 min. the printing time of the 3D models varies 10 h 12 min to 22 h 34 min. Conclusions The use of 3D printing technology has unquestionable potential applications to endoscopic endonasal approach for macroadenomas, in particular reflecting the complicated anatomy of sphenoid sinus and tumor location. Owing to the advantages of 3D printing technology, it may help the patients get a good prognosis.