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Aging-US: Knockdown of TXNDC9 induces apoptosis and autophagy in glioma

11-13-2020

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.

"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: prof_yunchen@yeah.net

Keywords: glioma, TXNDC9, apoptosis, autophagy, differentiation

About Aging-US:

Aging publishes research papers in all fields of aging research including but not limited, aging from yeast to mammals, cellular senescence, age-related diseases such as cancer and Alzheimer’s diseases and their prevention and treatment, anti-aging strategies and drug development and especially the role of signal transduction pathways such as mTOR in aging and potential approaches to modulate these signaling pathways to extend lifespan. The journal aims to promote treatment of age-related diseases by slowing down aging, validation of anti-aging drugs by treating age-related diseases, prevention of cancer by inhibiting aging. Cancer and COVID-19 are age-related diseases.

Aging is indexed by PubMed/Medline (abbreviated as “Aging (Albany NY)”), PubMed Central, Web of Science: Science Citation Index Expanded (abbreviated as “Aging‐US” and listed in the Cell Biology and Geriatrics & Gerontology categories), Scopus (abbreviated as “Aging” and listed in the Cell Biology and Aging categories), Biological Abstracts, BIOSIS Previews, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).

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