Aging-US: Knockdown of TXNDC9 induces apoptosis and autophagy in glioma11-13-2020
Aging-US recently published "Knockdown of TXNDC9 induces apoptosis and autophagy in glioma and mediates cell differentiation by p53 activation" which reported that no research associated with TXNDC9 has been reported in glioma.
In this study, the 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.
The apoptosis, autophagy, and cell differentiation program were blocked by p53 inhibitor treatment.
The Aging-US authors highlighted that, 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.
Dr. Yun Chen from The Peking University said, "Glioma is the most frequent primary tumor in the brain."
The proliferation of tumor cells is regulated by programmed cell death.
First discovered in 1960, mouse testicular teratoma cells could spontaneously differentiate into normal cells, then more and more studies have shown that dedifferentiated tumor cells can also be induced and re-differentiated into normal cells under the action of differentiation inducers, and their biological characteristics gradually move closer to normal cells and even transform into normal cells.
Figure 6. TXNDC9 regulated glioma autophagy and differentiation via controlling p53. (A) The level of LC3 and localization in U87 and U251 cells after si-TXNDC9/si-NC transfection, PFTα, and 3MA (5 mM) treatment. Representative immunofluorescence images were shown. (B) The protein level of Beclin-1 and LC3-I/II was detected in U87 and U251cells; Gapdh was indicated as a loading control. n= 6, *P<0.05. (C) U87 and U251 cell morphology were scanned after si-TXNDC9/si-NC transfection and PFTα treatment. (D) The protein level of vimentin and GFAP were measured in U87 and U251 cells, Gapdh was indicated as a loading control. n= 6, *P<0.05, **P<0.01.
It was reported that miR-146a/TRAF6 induced Th17 cell differentiation to control cervical cancer cell growth and apoptosis via NF-κB signaling.
EGFR/AKT signaling pathway involved in ovarian cancer cell differentiation via regulating TSA.
Knockdown of TXNDC9 could prevent tumor program, induce apoptosis, and autophagy in U87 and U251 cells.
The Chen Research Team concluded in their Aging-US Research Paper that, "for the first, the function of TXNDC9 was revealed in glioma cells. Knockdown of TXNDC induced apoptosis and autophagy of glioma cells and promoted differentiation through regulating p53."
Full Text - https://doi.org/10.18632/aging.103915
Correspondence to: Yun Chen email: email@example.com
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.