The redox regulator sulfiredoxin forms a complex with thioredoxin domain–containing 5 protein in response to ER stress in lung cancer cells

Chawsheen, Hedy A.; Jiang, Hong; Ying, Qi; Ding, Na; Thapa, Pratik; Wei, Qiou

doi:10.1074/jbc.ra118.005804

Cited by 14 publications

(21 citation statements)

References 41 publications

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“…A previous study indicated that TXNDC5 protects endothelial cells from stress-induced apoptosis (17). Similar effects were also observed in RA FLSs as evinced by both cell viability and inflammatory factor expression.…”

Section: Discussionsupporting

confidence: 70%

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TXNDC5 protects synovial fibroblasts of rheumatoid arthritis from the detrimental effects of endoplasmic reticulum stress

Wang

Zhang

et al. 2020

IRDR

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Section: Discussionsupporting

confidence: 70%

“…Intriguingly, a previous study found that TXNDC5 protects endothelial cells from stress-induced cell death. However, the exact role of TXNDC5 under ER stress remains unclear (17).…”

Section: Original Articlementioning

confidence: 99%

TXNDC5 protects synovial fibroblasts of rheumatoid arthritis from the detrimental effects of endoplasmic reticulum stress

Wang

Zhang

et al. 2020

IRDR

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“…The co-staining images of ASF1B (green fluorescence) and CDK9 (red fluorescence) indicated that ASF1B was present in the nucleus and co-localized with CDK9 in scrambled cells, and the immunofluorescent signal of CDK9 was also weak in the nucleus following ASF1B knockdown (Fig. 6i) 43 .…”

Section: Cdk9 Was Involved In the Progression Of Asf1b-mediated Hela mentioning

confidence: 97%

ASF1B promotes cervical cancer progression through stabilization of CDK9

et al. 2020

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Cervical cancer (CC) is one of the most deadly cancers in women, its current treatments still result in poor outcomes and developing the novel targets and therapeutic strategies are urgently needed. Recent studies have shown that anti-silencing function 1B (ASF1B) might be used as a new proliferation marker for cancer diagnosis and prognosis. However, the expression and function of ASF1B in cervical cancer remain unclear. Here, we induced ASF1B knockdown and overexpression in cervical cancer cell lines and detected the biological behavior changes in vitro. Furthermore, we established two murine models using stable ASF1B-shRNA HeLa cells or normal HeLa cells following AAV-shRNA-ASF1B administration to evaluate how suppression of ASF1B affects tumor growth. We showed that ASF1B functions as an oncogene in cervical cancer cells. Silence of ASF1B suppressed cervical cancer cell growth in vitro and in vivo, while, ASF1B overexpression accelerated cancer cell proliferation. Furthermore, ASF1B deficiency induced cell cycle arrest and apoptosis. Mechanistically, we found that ASF1B formed stable complexes with cyclin-dependent kinase 9 (CDK9), and positively regulated CDK9 stabilization. Taken together, tumorigenic ASF1B could be targeted to suppress cervical cancer tumor growth by inducing apoptotic cell death.

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“…[228] ER stress induces the association of sulfiredoxin with TXNDC5, and, depending on the levels of each, they have a different impact on cancer patient survival. [229] Inactivation of NR4A1 downregulates TXNDC5, thus promoting intracellular ROS and IL24 expression. This in turn inhibits the growth and induces apoptosis of rhabdomyosarcoma.…”

Section: Trx1/2mentioning

confidence: 99%

The NRF2, Thioredoxin, and Glutathione System in Tumorigenesis and Anticancer Therapies

et al. 2020

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Cancer remains an elusive, highly complex disease and a global burden. Constant change by acquired mutations and metabolic reprogramming contribute to the high inter- and intratumor heterogeneity of malignant cells, their selective growth advantage, and their resistance to anticancer therapies. In the modern era of integrative biomedicine, realizing that a personalized approach could benefit therapy treatments and patients’ prognosis, we should focus on cancer-driving advantageous modifications. Namely, reactive oxygen species (ROS), known to act as regulators of cellular metabolism and growth, exhibit both negative and positive activities, as do antioxidants with potential anticancer effects. Such complexity of oxidative homeostasis is sometimes overseen in the case of studies evaluating the effects of potential anticancer antioxidants. While cancer cells often produce more ROS due to their increased growth-favoring demands, numerous conventional anticancer therapies exploit this feature to ensure selective cancer cell death triggered by excessive ROS levels, also causing serious side effects. The activation of the cellular NRF2 (nuclear factor erythroid 2 like 2) pathway and induction of cytoprotective genes accompanies an increase in ROS levels. A plethora of specific targets, including those involved in thioredoxin (TRX) and glutathione (GSH) systems, are activated by NRF2. In this paper, we briefly review preclinical research findings on the interrelated roles of the NRF2 pathway and TRX and GSH systems, with focus given to clinical findings and their relevance in carcinogenesis and anticancer treatments.

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The redox regulator sulfiredoxin forms a complex with thioredoxin domain–containing 5 protein in response to ER stress in lung cancer cells

Cited by 14 publications

References 41 publications

TXNDC5 protects synovial fibroblasts of rheumatoid arthritis from the detrimental effects of endoplasmic reticulum stress

TXNDC5 protects synovial fibroblasts of rheumatoid arthritis from the detrimental effects of endoplasmic reticulum stress

ASF1B promotes cervical cancer progression through stabilization of CDK9

The NRF2, Thioredoxin, and Glutathione System in Tumorigenesis and Anticancer Therapies

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