Research Paper Volume 12, Issue 18 pp 18649—18659
Knockdown of TXNDC9 induces apoptosis and autophagy in glioma and mediates cell differentiation by p53 activation
- 1 Shenzhen Key Laboratory for Drug Addiction and Medication Safety, Department of Ultrasound, Peking University Shenzhen Hospital, Shenzhen Peking University, The Hong Kong University of Science and Technology Medical Center, Shenzhen, Guangdong Province, China
- 2 Clinical College of Shenzhen Hospital, Peking University, Anhui Medical University, Shenzhen, Guangdong Province, China
- 3 School of Materials Science and Engineering, Harbin Institute of Technology Shenzhen, Shenzhen, Guangdong Province, China
- 4 Queensland Micro- and Nanotechnology Centre, Griffith University, Brisbane, Australia
Received: April 17, 2020 Accepted: July 21, 2020 Published: September 8, 2020https://doi.org/10.18632/aging.103915
How to Cite
Copyright: © 2020 Zheng et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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.