&lt;p&gt;Low-Concentration PTX And RSL3 Inhibits Tumor Cell Growth Synergistically By Inducing Ferroptosis In Mutant p53 Hypopharyngeal Squamous Carcinoma&lt;/p&gt;

Ye, Jing; Jiang, Xiaohua; Dong, Zhihuai; Hu, Sideng; Xiao, Mang

doi:10.2147/cmar.s217944

Cited by 55 publications

(49 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Ye and his colleagues demonstrated that the combination of PTX and RSL3 rather than each agent alone induced ferroptosis in hypopharyngeal squamous carcinoma (HPSCC) cells with mutant p53 (mtp53) through the suppression of SLC7A11. mtp53 expression and, especially, the acetylation of K98 play a key role in PTX and RSL3-induced ferroptosis (33). In addition, a low dose of erastin can dramatically promote the therapeutic effects of cytarabine/ara-C and doxorubicin/adriamycin against leukemic cells in an RAS-independent manner that depends partly on ferroptosis induction.…”

Section: The Role Of Ferroptosis In Mainstream Cancer Treatments Ferrmentioning

confidence: 99%

Ferroptosis in Cancer Treatment: Another Way to Rome

Luo

et al. 2020

Front. Oncol.

118

View full text Add to dashboard Cite

Ferroptosis is a newly described type of programmed cell death and intensively related to both maintaining homeostasis and the development of diseases, especially cancers. Inducing ferroptosis leads to mitochondrial dysfunction and toxic lipid peroxidation in cells, which plays a pivotal role in suppressing cancer growth and progression. Here, we reviewed the existing studies about the molecular mechanisms of ferroptosis involved in different antitumor treatments, such as chemotherapy, targeted therapy, radiotherapy, and immunotherapy. We focused in particular on the distinct combinatorial therapeutic effects such as the synergistic sensitization effect and the drug-resistance reversal achieved when using ferroptosis inducers with conventional cancer therapy. Finally, we discussed the challenges and opportunities in clinical applications of ferroptosis. The application of nanotechnolgy and other novel technologies may provide a new direction in ferroptosis-driven cancer therapies.

show abstract

Section: The Role Of Ferroptosis In Mainstream Cancer Treatments Ferrmentioning

confidence: 99%

Ferroptosis in Cancer Treatment: Another Way to Rome

Luo

et al. 2020

Front. Oncol.

118

View full text Add to dashboard Cite

show abstract

“…SLC7A11 is a major component of System X C − and the latter is indispensable for importing cystine, which is used to synthesize antioxidant GSH [19,44]. Previous studies have demonstrated that p53 directs the transcriptionally suppressed SLC7A11 expression [41,45,46], thereby suppressing system X C − activity to trigger ferroptosis. In a similar mechanism depicted in Fig.…”

Section: Discussionmentioning

confidence: 99%

LncRNA-MEG3 functions as ferroptotic promoter to mediate OGD combined high glucose-induced death of rat brain microvascular endothelial cells via the p53-GPX4 axis

Chen¹,

Huang²,

Xia³

et al. 2020

Preprint

View full text Add to dashboard Cite

Background Individuals with diabetes are exposed to a higher risk of perioperative stroke than non-diabetics mainly due to persistent hyperglycemia. lncRNA-MEG3 (long non-coding RNA maternally expressed gene 3) has been considered as an important mediator in regulating ischemic stroke. However, the functional and regulatory roles of lncRNA-MEG3 in diabetic brain ischemic injury remain unclear. Results In this study, RBMVECs (the rat brain microvascular endothelial cells) were exposed to 6 h of OGD (oxygen and glucose deprivation), and subsequent reperfusion via incubating cells with glucose of various high concentrations for 24 h to imitate in vitro diabetic brain ischemic injury. It was shown that the marker events of ferroptosis and increased lncRNA-MEG3 expression occurred after the injury induced by OGD combined with hyperglycemic treatment. However, all ferroptotic events were reversed with the treatment of MEG3-siRNA. Moreover, in this in vitro model, p53 was also characterized as a downstream target of lncRNA-MEG3. Furthermore, p53 knockdown protected RBMVECs against OGD + hyperglycemic reperfusion-induced ferroptosis, while the overexpression of p53 exerted opposite effects, implying that p53 served as a positive regulator of ferroptosis. Additionally, the overexpression or knockdown of p53 significantly modulated GPX4 expression in RBMVECs exposed to the injury induced by OGD combined with hyperglycemic treatment. Furthermore, GPX4 expression was suppressed again after the introduction of p53 into cells silenced by lncRNA-MEG3. Finally, ChIP assay uncovered that p53 was bound to GPX4 promoter. Conclusions Altogether, these data revealed that, by modulating GPX4 transcription and expression, the lncRNA-MEG3-p53 signaling pathway mediated the ferroptosis of RBMVECs upon injury induced by OGD combined with hyperglycemic treatment.

show abstract

“…5c). Ye et al 241 investigated the effect of the combined administration of paclitaxel and RSL3: alone and at low concentrations, these agents do not cause substantial cell death. Low-concentration paclitaxel (3-6 nM) is reported to interfere with glutaminolysis, a process that is essential for ferroptosis.…”

Section: Drug Combinationsmentioning

confidence: 99%

Cysteine metabolic circuitries: druggable targets in cancer

et al. 2020

View full text Add to dashboard Cite

To enable survival in adverse conditions, cancer cells undergo global metabolic adaptations. The amino acid cysteine actively contributes to cancer metabolic remodelling on three different levels: first, in its free form, in redox control, as a component of the antioxidant glutathione or its involvement in protein s-cysteinylation, a reversible post-translational modification; second, as a substrate for the production of hydrogen sulphide (H2S), which feeds the mitochondrial electron transfer chain and mediates per-sulphidation of ATPase and glycolytic enzymes, thereby stimulating cellular bioenergetics; and, finally, as a carbon source for epigenetic regulation, biomass production and energy production. This review will provide a systematic portrayal of the role of cysteine in cancer biology as a source of carbon and sulphur atoms, the pivotal role of cysteine in different metabolic pathways and the importance of H2S as an energetic substrate and signalling molecule. The different pools of cysteine in the cell and within the body, and their putative use as prognostic cancer markers will be also addressed. Finally, we will discuss the pharmacological means and potential of targeting cysteine metabolism for the treatment of cancer.

show abstract

<p>Low-Concentration PTX And RSL3 Inhibits Tumor Cell Growth Synergistically By Inducing Ferroptosis In Mutant p53 Hypopharyngeal Squamous Carcinoma</p>

Cited by 55 publications

References 36 publications

Ferroptosis in Cancer Treatment: Another Way to Rome

Ferroptosis in Cancer Treatment: Another Way to Rome

LncRNA-MEG3 functions as ferroptotic promoter to mediate OGD combined high glucose-induced death of rat brain microvascular endothelial cells via the p53-GPX4 axis

Cysteine metabolic circuitries: druggable targets in cancer

Contact Info

Product

Resources

About