Abstract
Glioma is the most common malignant brain tumor. Because of its high degree of malignancy, the effect of surgical treatment, radiotherapy, chemotherapy, or immunotherapy is not ideal. TXNDC9 belongs to thioredoxin domain-containing proteins, which is involved in tumor progression. However, no research associated with TXNDC9 has been reported in glioma. In this study, we found that TXNDC9 was upregulated in glioma. Knockdown of TXNDC9 would prevent proliferation and metastasis, induce the apoptosis rate of glioma cells, and promote the expression Cleaved-caspase3, Cleaved-caspase8, Cleaved-caspase9. Meanwhile, knockdown of TXNDC9 induced autophagy by increasing the level of LC3 and Beclin-1. Cell morphology and expression analysis of GFAP, Vimentin, verified that TXNDC9 could regulate glioma cell differentiation. During this program, the expression of p53 changes dramatically. The apoptosis, autophagy, and cell differentiation program were blocked by p53 inhibitor treatment. In conclusion, the silencing of TXNDC9 induces apoptosis and autophagy in glioma and promotes cell differentiation by controlling p53 and may function as a new mechanism in glioma.
Highlights
Glioma is the most frequent primary tumor in the brain [1]
The results showed that the mRNA and protein expression level of Thioredoxin domain-containing 9 (TXNDC9) was an upregulation in tumors compared with normal tissues (Figure 1A, 1B)
Compared with NHA, the expression of TXNDC9 was up-regulated in all glioma cell lines (Figure 1C, 1D)
Summary
Glioma is the most frequent primary tumor in the brain [1]. It has the characteristics of high incidence, invasive growth, and recurrence [2, 3]. The proliferation of tumor cells is regulated by programmed cell death. Autophagy and apoptosis are two forms of programmed cell death [4]. They have significant differences in morphology and function, but there are many connections, which are related to the activation, expression, and regulation of a series of genes. Whether autophagy can be regulated or not is closely related to the growth and apoptosis of tumor cells
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
