Nuclear receptor coactivator 4-mediated ferritinophagy drives proliferation of dental pulp stem cells in hypoxia

Yang, Andi; Wang, Lulu; Jiang, Ke; Lei, Lang; Li, Houxuan

doi:10.1016/j.bbrc.2021.03.075

Cited by 7 publications

(6 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The alteration of iron in HCC cells directly increased LPO through the Fenton reaction, leading to ferroptosis of HCC cells [ 60 ]. Similarly, Yang et al [ 61 ] reported that p38 activation was involved in upregulation of NCOA4 and downregulation of FTH1 in dental pulp stem cells, which was consistent with our results. In our study, FTH1 was decreased by anisomycin at both protein and RNA level in Figures 1(e) and 6(b) .…”

Section: Discussionsupporting

confidence: 93%

Modulation of the p38 MAPK Pathway by Anisomycin Promotes Ferroptosis of Hepatocellular Carcinoma through Phosphorylation of H3S10

Chen

Yang

Zhang

et al. 2022

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

Hepatocellular carcinoma (HCC) is a prevalent malignant tumor worldwide. Ferroptosis is emerging as an effective target for tumor treatment as it has been shown to potentiate cell death in some malignancies. However, it remains unclear whether histone phosphorylation events, an epigenetic mechanism that regulates transcriptional expression, are involved in ferroptosis. Our study found that supplementation with anisomycin, an agonist of p38 mitogen-activated protein kinase (MAPK), induced ferroptosis in HCC cells, and the phosphorylation of histone H3 on serine 10 (p-H3S10) was participated in anisomycin-induced ferroptosis. To investigate the anticancer effects of anisomycin-activated p38 MAPK in HCC, we analyzed cell viability, colony formation, cell death, and cell migration in Hep3B and HCCLM3 cells. The results showed that anisomycin could significantly suppress HCC cell colony formation and migration and induce HCC cell death. The hallmarks of ferroptosis, such as abnormal accumulation of iron and elevated levels of lipid peroxidation and malondialdehyde, were detected to confirm the ability of anisomycin to promote ferroptosis. Furthermore, coincubation with SB203580, an inhibitor of activated p38 MAPK, partially rescued anisomycin-induced ferroptosis. And the levels of p-p38 MAPK and p-H3S10 were successively increased by anisomycin treatment. The relationship between p-H3S10 and ferroptosis was revealed by ChIP sequencing. The reverse transcription PCR and immunofluorescence results showed that NCOA4 was upregulated both in mRNA and protein levels after anisomycin treatment. And by C11-BODIPY staining, we found that anisomycin-induced lipid reactive oxygen species was reduced after NCOA4 knockdown. In conclusion, the anisomycin-activated p38 MAPK promoted ferroptosis of HCC cells through H3S10 phosphorylation.

show abstract

Section: Discussionsupporting

confidence: 93%

Modulation of the p38 MAPK Pathway by Anisomycin Promotes Ferroptosis of Hepatocellular Carcinoma through Phosphorylation of H3S10

Chen

Yang

Zhang

et al. 2022

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

show abstract

“…This could be a consequence of the stemnessmaintaining effects of hypoxia. Recent studies have shown that hypoxia can stimulate the proliferation of dermal papilla cells [23] , dental pulp stem cells [24] , neural stem cells [25] , and mesenchymal stem cells [26] , among others [27][28][29] . To some extent, dermal papilla cells can be considered a unique source of mesenchymal stem cells [30] .…”

Section: Discussionmentioning

confidence: 99%

“…As this self-renewal process significantly enlarges stem cell pools, the proliferation-promoting effect of hypoxia could increase tissue density rather than tissue volume. Specifically, our results showed that hypoxia decreased the PAX6-and CHX10-positive RPCs ratio [22][23][24][25][26][27][28][29][30][31][32][33][34] . A previous study using the adherent differentiation method to generate RPCs showed that a low-oxygen environment could increase the percentage of RPCs co-expressing PAX6 and CHX10 [35] .…”

Section: Discussionmentioning

confidence: 99%

Influence of hypoxia on retinal progenitor and ganglion cells in human induced pluripotent stem cell-derived retinal organoids

Du,

Wang,

et al. 2023

Int J Ophthalmol

View full text Add to dashboard Cite

AIM: To observe the effect of low oxygen concentration on the neural retina in human induced pluripotent stem cell (hiPSC)-derived retinal organoids (ROs). METHODS: The hiPSC and a three-dimensional culture method were used for the experiments. Generated embryoid bodies (EBs) were randomly and equally divided into hypoxic and normoxic groups. Photographs of the EBs were taken on days 38, 45, and 52, and the corresponding volume of EBs was calculated. Simultaneously, samples were collected at these three timepoints, followed by fixation, sectioning, and immunofluorescence. RESULTS: The proportion of Ki67-positive proliferating cells increased steadily on day 38; this proliferation-promoting effect tended to increase tissue density rather than tissue volume. On days 45 and 52, the two groups had relatively similar ratios of Ki67-positive cells. Further immunofluorescence analysis showed that the ratio of SOX2-positive cells significantly increased within the neural retina on day 52 (P<0.05). In contrast, the percentage of PAX6- and CHX10-positive cells significantly decreased following hypoxia treatment at all three timepoints (P<0.01), except for CHX10 at day 45 (P>0.05). Moreover, the proportion of PAX6-/TUJ1+ cells within the neural retinas increased considerably (P<0.01, <0.05, <0.05 respectively). CONCLUSION: Low oxygen promotes stemness and proliferation of neural retinas, suggesting that hypoxic conditions can enlarge the retinal progenitor cell pool in hiPSC-derived ROs.

show abstract

“…After entering cells via the transferrin receptor 1 (TfR1) on the cell membrane, Fe 3+ is deoxidized and converted to Fe 2+ under the action of iron oxide reductase six transmembrane epithelial antigen of the prostate 3 (STEAP3) ( 72 ). After that, Fe 2+ is transported to the labile iron pool (LIP) in the cytoplasm by divalent metal transporter 1 (DMT1) ( 73 ). Intracellular iron is mainly stored in ferritin, and the autophagic degradation of ferritin, which is mediated by nuclear receptor coactivator 4 (NCOA4) ( 74 ), can release iron into LIP.…”

Section: Ferroptosismentioning

confidence: 99%

Ferroptosis open a new door for colorectal cancer treatment

Liang

Tong

et al. 2023

Front. Oncol.

View full text Add to dashboard Cite

Colorectal cancer (CRC) is the third highest incidence and the second highest mortality malignant tumor in the world. The etiology and pathogenesis of CRC are complex. Due to the long course of the disease and no obvious early symptoms, most patients are diagnosed as middle and late stages. CRC is prone to metastasis, most commonly liver metastasis, which is one of the leading causes of death in CRC patients. Ferroptosis is a newly discovered cell death form with iron dependence, which is driven by excessive lipid peroxides on the cell membrane. It is different from other form of programmed cell death in morphology and mechanism, such as apoptosis, pyroptosis and necroptosis. Numerous studies have shown that ferroptosis may play an important role in the development of CRC. For advanced or metastatic CRC, ferroptosis promises to open a new door in the setting of poor response to chemotherapy and targeted therapy. This mini review focuses on the pathogenesis of CRC, the mechanism of ferroptosis and the research status of ferroptosis in CRC treatment. The potential association between ferroptosis and CRC and some challenges are discussed.

show abstract

Nuclear receptor coactivator 4-mediated ferritinophagy drives proliferation of dental pulp stem cells in hypoxia

Cited by 7 publications

References 29 publications

Modulation of the p38 MAPK Pathway by Anisomycin Promotes Ferroptosis of Hepatocellular Carcinoma through Phosphorylation of H3S10

Modulation of the p38 MAPK Pathway by Anisomycin Promotes Ferroptosis of Hepatocellular Carcinoma through Phosphorylation of H3S10

Influence of hypoxia on retinal progenitor and ganglion cells in human induced pluripotent stem cell-derived retinal organoids

Ferroptosis open a new door for colorectal cancer treatment

Contact Info

Product

Resources

About