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  • Springer Science and Business Media LLC  (7)
  • 2020-2024  (7)
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  • Springer Science and Business Media LLC  (7)
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  • 2020-2024  (7)
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  • 1
    Online Resource
    Online Resource
    RIPK1-dependent necroptosis promotes vasculogenic mimicry formation via eIF4E in triple-negative breast cancer
    Springer Science and Business Media LLC ; 2023
    In:  Cell Death & Disease Vol. 14, No. 5 ( 2023-05-22)
    Details
    In: Cell Death & Disease, Springer Science and Business Media LLC, Vol. 14, No. 5 ( 2023-05-22)
    Abstract: Necroptosis is a caspase-independent form of programmed cell death. Receptor interacting protein kinase 1 (RIPK1) is a key molecule in the initiation of necroptosis and the formation of the necrotic complex. Vasculogenic mimicry (VM) provides a blood supply to tumor cells that is not dependent on endothelial cells. However, the relationship between necroptosis and VM in triple-negative breast cancer (TNBC) is not fully understood. In this study, we found that RIPK1-dependent necroptosis promoted VM formation in TNBC. Knockdown of RIPK1 significantly suppressed the number of necroptotic cells and VM formation. Moreover, RIPK1 activated the p-AKT/eIF4E signaling pathway during necroptosis in TNBC. eIF4E was blocked by knockdown of RIPK1 or AKT inhibitors. Furthermore, we found that eIF4E promoted VM formation by promoting epithelial-mesenchymal transition (EMT) and the expression and activity of MMP2. In addition to its critical role in necroptosis-mediated VM, eIF4E was essential for VM formation. Knockdown of eIF4E significantly suppressed VM formation during necroptosis. Finally, through clinical significance, the results found that eIF4E expression in TNBC was positively correlated with the mesenchymal marker vimentin, the VM marker MMP2, and the necroptosis markers MLKL and AKT. In conclusion, RIPK1-dependent necroptosis promotes VM formation in TNBC. Necroptosis promotes VM formation by activating RIPK1/p-AKT/eIF4E signaling in TNBC. eIF4E promotes EMT and MMP2 expression and activity, leading to VM formation. Our study provides a rationale for necroptosis-mediated VM and also providing a potential therapeutic target for TNBC.
    Type of Medium: Online Resource
    ISSN: 2041-4889
    URL: Article
    DOI: 10.1038/s41419-023-05841-w
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2023
    detail.hit.zdb_id: 2541626-1
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  • 2
    Online Resource
    Online Resource
    Irbesartan overcomes gemcitabine resistance in pancreatic cancer by suppressing stemness and iron metabolism via inhibition of the Hippo/YAP1/c-Jun axis
    Springer Science and Business Media LLC ; 2023
    In:  Journal of Experimental & Clinical Cancer Research Vol. 42, No. 1 ( 2023-05-04)
    Details
    In: Journal of Experimental & Clinical Cancer Research, Springer Science and Business Media LLC, Vol. 42, No. 1 ( 2023-05-04)
    Abstract: Chemoresistance is the main reason for the poor prognosis of pancreatic ductal adenocarcinoma (PDAC). Thus, there is an urgent need to screen out new targets and compounds to reverse chemotherapeutic resistance. Methods We established a bio-bank of human PDAC organoid models, covering a representative range of PDAC tumor subtypes. We screened a library of 1304 FDA-approved compounds to identify candidates efficiently overcoming chemotherapy resistance. The effects of the compounds were evaluated with a CellTiter-Glo-3D assay, organoid apoptosis assay and in vivo patient-derived xenograft (PDX), patient-derived organoid (PDO) and LSL-Kras G12D/+ ; LSL-Trp53 R172H/+ ; Pdx1-Cre (KPC) genetically engineered mouse models. RNA-sequencing, genome editing, sphere formation assays, iron assays and luciferase assays were conducted to elucidate the mechanism. Results High-throughput drug screening of chemotherapy-resistant PDOs identified irbesartan, an angiotensin ‖ type 1 (AT1) receptor antagonist, which could synergistically enhance the ability of chemotherapy to kill PDAC cells. In vitro and in vivo validation using PDO, PDX and KPC mouse models showed that irbesartan efficiently sensitized PDAC tumors to chemotherapy. Mechanistically, we found that irbesartan decreased c-Jun expression by inhibiting the Hippo/YAP1 pathway and further overcame chemotherapy resistance in PDAC. We also explored c-Jun, a potential target of irbesartan, which can transcriptionally upregulate the expression of key genes involved in stemness maintenance (SOX9/SOX2/OCT4) and iron metabolism (FTH1/FTL/TFRC). More importantly, we observed that PDAC patients with high levels of c-Jun expression demonstrated poor responses to the current standard chemotherapy regimen (gemcitabine plus nab-paclitaxel). Moreover, patients with PDAC had significant survival benefits from treatment with irbesartan plus a standard chemotherapy regimen in two-center retrospective clinical cohorts and patients with high c-Jun expression exhibited a better response to combination chemotherapy. Conclusions Irbesartan could be used in combination with chemotherapy to improve the therapeutic efficacy in PDAC patients with high levels of c-Jun expression. Irbesartan effectively inhibited chemotherapy resistance by suppressing the Hippo/YAP1/c-Jun/stemness/iron metabolism axis. Based on our findings, we are designing an investigator-initiated phase II clinical trial on the efficacy and safety of irbesartan plus a standard gemcitabine/nab-paclitaxel regimen in the treatment of patients with advanced III/IV staged PDAC and are hopeful that we will observe patient benefits.
    Type of Medium: Online Resource
    ISSN: 1756-9966
    URL: Article
    DOI: 10.1186/s13046-023-02671-8
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2023
    detail.hit.zdb_id: 2430698-8
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  • 3
    Online Resource
    Online Resource
    Correction: RIPK1-dependent necroptosis promotes vasculogenic mimicry formation via eIF4E in triple-negative breast cancer
    Springer Science and Business Media LLC ; 2023
    In:  Cell Death & Disease Vol. 14, No. 9 ( 2023-09-14)
    Details
    In: Cell Death & Disease, Springer Science and Business Media LLC, Vol. 14, No. 9 ( 2023-09-14)
    Type of Medium: Online Resource
    ISSN: 2041-4889
    URL: Article
    DOI: 10.1038/s41419-023-06052-z
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2023
    detail.hit.zdb_id: 2541626-1
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  • 4
    Online Resource
    Online Resource
    Characteristics of the Cretaceous Magmatism in Huanghua Depression and Their Relationships with Hydrocarbon Enrichment
    Springer Science and Business Media LLC ; 2020
    In:  Journal of Earth Science Vol. 31, No. 6 ( 2020-12), p. 1273-1292
    Details
    In: Journal of Earth Science, Springer Science and Business Media LLC, Vol. 31, No. 6 ( 2020-12), p. 1273-1292
    Type of Medium: Online Resource
    ISSN: 1674-487X , 1867-111X
    URL: Article
    DOI: 10.1007/s12583-020-1308-8
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2020
    detail.hit.zdb_id: 2501172-8
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  • 5
    Online Resource
    Online Resource
    ESE3-positive PSCs drive pancreatic cancer fibrosis, chemoresistance and poor prognosis via tumour–stromal IL-1β/NF–κB/ESE3 signalling axis
    Springer Science and Business Media LLC ; 2022
    In:  British Journal of Cancer Vol. 127, No. 8 ( 2022-11-01), p. 1461-1472
    Details
    In: British Journal of Cancer, Springer Science and Business Media LLC, Vol. 127, No. 8 ( 2022-11-01), p. 1461-1472
    Abstract: Desmoplastic stroma, a feature of pancreatic ductal adenocarcinoma (PDAC), contains abundant activated pancreatic stellate cells (PSCs). How PSCs promote PDAC progression remains incompletely understood. Methods Effect of epithelium-specific E-twenty six factor 3 (ESE3)-positive PSCs on PDAC fibrosis and chemoresistance was examined by western blot, RT-PCR, immunofluorescence, flow cytometry assay, chromatin immunoprecipitation, luciferase assay, immunohistochemistry and subcutaneous pancreatic cancer mouse model. Results ESE3 expression increased in PSCs in PDAC tissues compared with those in normal PSCs. Clinical data showed that ESE3 upregulation in PSCs was positively correlated with tumour size, pTNM stage, CA19-9, carcinoembryonic antigen and serum CA242 level. ESE3 overexpression in PSCs was an independent negative prognostic factor for disease-free survival and overall survival amongst patients with PDAC. Mechanistically, the conditional medium from the loss and gain of ESE3-expressing PSCs influenced PDAC chemoresistance and tumour growth. ESE3 directly induced the transcription of α-SMA, collagen-I and IL-1β by binding to ESE3-binding sites on their promoters to activate PSCs. IL-1β upregulated ESE3 in PSCs through NF-κB activation, and ESE3 was required for PSC activation by tumour cell-derived IL-1β. Conclusion Inhibiting the IL-1β/ESE3 (PSCs)/IL-1β-positive feedback loop is a promising therapeutic strategy to reduce tumour fibrosis and increase chemotherapeutic efficacy in PDAC.
    Type of Medium: Online Resource
    ISSN: 0007-0920 , 1532-1827
    URL: Article
    DOI: 10.1038/s41416-022-01927-y
    RVK:
    XA 33500
    RVK:
    XA 10000
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2022
    detail.hit.zdb_id: 2002452-6
    detail.hit.zdb_id: 80075-2
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  • 6
    Online Resource
    Online Resource
    Study of a Si-based light initiated multi-gate semiconductor switch for high temperatures
    Springer Science and Business Media LLC ; 2022
    In:  Scientific Reports Vol. 12, No. 1 ( 2022-09-15)
    Details
    In: Scientific Reports, Springer Science and Business Media LLC, Vol. 12, No. 1 ( 2022-09-15)
    Abstract: Light initiated multi-gate semiconductor switch (LIMS) is a kind of power electronic device which has many differences from traditional thyristor triggered by electric pulse. LIMS is triggered by laser, the turn-on time is smaller, and the anti-electromagnetic interferences is strong. The opening mode of LIMS is obviously different to traditional thyristor. After the laser into the gate area, a large number of electrons and holes will appear in P-base region, holes gather in the area of P-base in PN junction J2, and electrons gather in N-drift region around the PN junction J2. PN junction J2 will open first, then PN junction J3 opens. The delay time of the NPN and PNP thyristors is close to zero when the laser pulse is narrow and the peak power is high, so the turn-on velocity is fast. To optimize the characteristics of the LIMS at high temperatures, we propose a new structure of the LIMS with the optimization of the n + layer, circular light gate, and the new-style edge termination. The diameter of the LIMS is 23 mm. The experiment results show that the leakage current of the proposed LIMS has been decreased from more than 1 mA to 500 μA at 125 °C, the output current of the LIMS is 10.2 kA with a voltage of 4 kV at 85 °C, and the output current of the LIMS is 12.1 kA with a voltage of 4 kV at − 55 °C. Additionally, di/dt is larger than 30 kA/μs.
    Type of Medium: Online Resource
    ISSN: 2045-2322
    URL: Article
    DOI: 10.1038/s41598-022-19767-4
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2022
    detail.hit.zdb_id: 2615211-3
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  • 7
    Online Resource
    Online Resource
    BICC1 drives pancreatic cancer progression by inducing VEGF-independent angiogenesis
    Springer Science and Business Media LLC ; 2023
    In:  Signal Transduction and Targeted Therapy Vol. 8, No. 1 ( 2023-07-14)
    Details
    In: Signal Transduction and Targeted Therapy, Springer Science and Business Media LLC, Vol. 8, No. 1 ( 2023-07-14)
    Abstract: VEGF inhibitors are one of the most successful antiangiogenic drugs in the treatment of many solid tumors. Nevertheless, pancreatic adenocarcinoma (PAAD) cells can reinstate tumor angiogenesis via activation of VEGF-independent pathways, thereby conferring resistance to VEGF inhibitors. Bioinformatic analysis showed that BICC1 was one of the top genes involved in the specific angiogenesis process of PAAD. The analysis of our own cohort confirmed that BICC1 was overexpressed in human PAAD tissues and was correlated to increased microvessel density and tumor growth, and worse prognosis. In cells and mice with xenograft tumors, BICC1 facilitated angiogenesis in pancreatic cancer in a VEGF-independent manner. Mechanistically, as an RNA binding protein, BICC1 bounds to the 3’UTR of Lipocalin-2 (LCN2) mRNA and post-transcriptionally up-regulated LCN2 expression in PAAD cells. When its level is elevated, LCN2 binds to its receptor 24p3R, which directly phosphorylates JAK2 and activates JAK2/STAT3 signal, leading to increased production of an angiogenic factor CXCL1. Blocking of the BICC1/LCN2 signalling reduced the microvessel density and tumor volume of PAAD cell grafts in mice, and increased the tumor suppressive effect of gemcitabine. In conclusion, BICC1 plays a pivotal role in the process of VEGF-independent angiogenesis in pancreatic cancer, leading to resistance to VEGF inhibitors. BICC1/LCN2 signaling may serve as a promising anti-angiogenic therapeutic target for pancreatic cancer patients.
    Type of Medium: Online Resource
    ISSN: 2059-3635
    URL: Article
    DOI: 10.1038/s41392-023-01478-5
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2023
    detail.hit.zdb_id: 2886872-9
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