<scp>FAS</scp> and <scp>RAS</scp> related Apoptosis defects: From autoimmunity to leukemia

Meynier, Sonia; Rieux-Laucat, Frédéric

doi:10.1111/imr.12720

Cited by 50 publications

(23 citation statements)

References 97 publications

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“…In G6PD-deficient melanoma cells, the expression of Bcl-2 and Bcl-xL is significantly reduced. Fas, a death domain-containing protein regulating programmed cell death, is highly expressed in G6PD-deficient melanoma cells [160]. The protein expression of the STAT3/5 ratio and the phosphorylated STAT3/5 ratio are decreased in G6PD-deficient melanoma cells.…”

Section: The Role Of G6pd In Cell Growth and Developmentmentioning

confidence: 99%

The Redox Role of G6PD in Cell Growth, Cell Death, and Cancer

Yang

Yen

et al. 2019

Cells

157

132

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The generation of reducing equivalent NADPH via glucose-6-phosphate dehydrogenase (G6PD) is critical for the maintenance of redox homeostasis and reductive biosynthesis in cells. NADPH also plays key roles in cellular processes mediated by redox signaling. Insufficient G6PD activity predisposes cells to growth retardation and demise. Severely lacking G6PD impairs embryonic development and delays organismal growth. Altered G6PD activity is associated with pathophysiology, such as autophagy, insulin resistance, infection, inflammation, as well as diabetes and hypertension. Aberrant activation of G6PD leads to enhanced cell proliferation and adaptation in many types of cancers. The present review aims to update the existing knowledge concerning G6PD and emphasizes how G6PD modulates redox signaling and affects cell survival and demise, particularly in diseases such as cancer. Exploiting G6PD as a potential drug target against cancer is also discussed.

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Section: The Role Of G6pd In Cell Growth and Developmentmentioning

confidence: 99%

The Redox Role of G6PD in Cell Growth, Cell Death, and Cancer

Yang

Yen

et al. 2019

Cells

157

132

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“…The changes include a strong upregulation of a number of proapoptotic genes, such as FAS, TNFSF10/TRAIL, PUMA, NOXA, BAX, and AEN, and downregulation of antiapoptotic proteins such as survivin/BIRC5 and BCL-2. FAS and TRAIL are components of the extrinsic pathway of apoptosis and themselves are attractive therapeutic targets (41,42), whereas the others are key regulators of the intrinsic pathway. PUMA, NOXA, BAX, AEN, FAS, and TRAIL are established direct targets of p53 (43), thus indicating a strong activation of p53 proapoptosis function by the combination treatment.…”

Section: Discussionmentioning

confidence: 99%

Therapeutic Targeting of MDR1 Expression by RORγ Antagonists Resensitizes Cross-Resistant CRPC to Taxane via Coordinated Induction of Cell Death Programs

Wang

Huang

Chen

et al. 2020

Molecular Cancer Therapeutics

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Overexpression of ATP-binding cassette subfamily B member 1 (ABCB1)-encoded multidrug resistance protein 1 (MDR1) constitutes a major mechanism of cancer drug resistance including docetaxel (DTX) and cabazitaxel (CTX) resistance in castrationresistant prostate cancer (CRPC). However, no therapeutics that targets MDR1 is available at clinic for taxane sensitization. We report here that retinoic acid receptor-related orphan receptor g (RORg), a nuclear receptor family member, unexpectedly mediates MDR1/ABCB1 overexpression. RORg plays an important role in controlling the functions of subsets of immune cells and has been an attractive target for autoimmune diseases. We found that its small-molecule antagonists are efficacious in resensitizing DTX and CTX cross-resistant CRPC cells and tumors to taxanes in both androgen receptor-positive and-negative models. Our mechanistic analyses revealed that combined treatment with RORg antagonists and taxane elicited a robust synergy in killing the resistant cells, which involves a coordinated alteration of p53, Myc, and E2F-controlled programs critical for both intrinsic and extrinsic apoptosis, survival, and cell growth. Our results suggest that targeting RORg with small-molecule inhibitors is a novel strategy for chemotherapy resensitization in tumors with MDR1 overexpression.

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“…Hsa-miR-181c-5p down-regulated the expression of FAS, promoted the proliferation and inhibited the apoptosis of hNPCs As a member of the TNF receptor super-family, the protein encoded by FAS plays a central role in the physiological regulation of programmed cell death, and has been involved in the onset of various malignant tumors and immune system diseases [19][20][21]. The bioinformatics prediction results showed that FAS was a potential target of hsa-miR-181c-5p (Figure 4A).…”

Section: Hsa_circ_0001658 Acted As a Sponge Of Hsa-mir-181c-5pmentioning

confidence: 99%

Circular RNA hsa_circ_0001658 Inhibits Intervertebral Disc Degeneration Development by Regulating hsa-miR-181c-5p/FAS

Meng

2021

Preprint

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Background and purpose: Intervertebral disc degeneration (IDD) is the main cause of low back pain, but its pathogenesis has not been studied clearly. Circular RNA is a type of non-coding RNA (ncRNA). In this study, we aim to study the potential role of circular RNA in the pathogenesis of IDD. Methods: We obtained microarray data (GSE116726, GSE67566) from Gene Expression Omnibus database, and differentially analyzed ncRNA in nucleus pulposus (NP) tissues of IDD patients. The potential circRNAs-miRNAs-mRNAs regulatory network was analyzed by starBase. The effect of the interaction between hsa_circ_0001658, hsa-miR-181c-5p and FAS on the proliferation and apoptosis of human neural progenitor cells (hNPCs) were studied. Results:Hsa_circ_0001658 was significantly up-regulated (logFC>2.0 and adj.P.Val<0.01) in the NP tissues of IDD patients, and hsa-miR-181c-5p expression was down-regulated (logFC<-2.0 and adj.P.Val<0.01). Silencing of hsa-miR-181c-5p or overexpression of hsa_circ_0001658 inhibited the proliferation of hNPCs and promoted their apoptosis. Hsa_circ_0001658 acted as a sponge of hsa-miR-181c-5p. Hsa-miR-181c-5p down-regulated the expression of FAS, promoted the proliferation and inhibited the apoptosis of hNPCs. Hsa_circ_0001658 functioned in hNPCs through targeting hsa-miR-181c-5p/FAS.Conclusion:Circular RNA hsa_circ_0001658 inhibits intervertebral disc degeneration development by regulating hsa-miR-181c-5p/FAS. It is expected to be a potential target for the therapy of IDD.

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FAS and RAS related Apoptosis defects: From autoimmunity to leukemia

Cited by 50 publications

References 97 publications

The Redox Role of G6PD in Cell Growth, Cell Death, and Cancer

The Redox Role of G6PD in Cell Growth, Cell Death, and Cancer

Therapeutic Targeting of MDR1 Expression by RORγ Antagonists Resensitizes Cross-Resistant CRPC to Taxane via Coordinated Induction of Cell Death Programs

Circular RNA hsa_circ_0001658 Inhibits Intervertebral Disc Degeneration Development by Regulating hsa-miR-181c-5p/FAS

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