<p>Glioma is the most common and aggressive primary adult brain tumor. Furthermore, the prognosis for glioma patients following chemoradiotherapy is unfavourable due to the inherent anti-apoptotic characteristics of glioma cells. Thus, the treatment of gliomas remains a challenge. Our aim was to define the molecular mechanisms underlying the effects of TXN1 on the anti-apoptotic ability and proliferation of glioma cells. The relationship between TXN1 expression and glioma patients was initially predicted using bioinformatics methods and then verified through clinical glioma tissue Results showed that the expression of TXN1 increases with the malignant degree of glioma, leading to a worse prognosis for patients.Then glioma cells were treated with lentivirus to be stable cell lines with suppressed TXN1 expression. MTT, flow cytometry, immunofluorescence, western blot and qRT-PCR were used to analyse changes in glioma proliferation, cell cycle, apoptosis and the expressioin of the P38 MAPK signaling pathway. Moreover,the expression levels of related proteins in the transplanted tumor tissues of nude mice were investigated by immunohistochemistry. Reducing TXN1 expression caused glioma cell cycle in G2/M phase, increased cell apoptosis rate and mitochondrial membrane damage. Furthermore, this was correlated with activity of the P38 MAPK pathway. Reduction of TXN1 expression can activate the P38 MAPK pathway to cause glioma cell cycle arrest and induce mitochondrial apoptosis. This study revealed for the first time that inhibition of TXN1 can destroy the apoptotic resistance mechanism of glioma by activating ASK1/P38 MAPK axis, resulting in G2/M phase arrest of glioma cells, inhibiting the proliferation of glioma cells, and promoting apoptosis of glioma cells in malignant gliomas. Combining TXN1 inhibitors with radiotherapy and chemotherapy is expected to significantly improve the clinical prognosis of glioma patients.</p>