PKR deficiency delays vascular aging via inhibiting GSDMD-mediated endothelial cell hyperactivation

Peng, Zhouyangfan; Tan, Xiqing; Xie, Liangpeng; Li, Ze; Zhou, Sufang; Li, Yapei

doi:10.1016/j.isci.2022.105909

Cited by 2 publications

(2 citation statements)

References 27 publications

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“…For other CSC-associated proteins, such as SOX2, OCT4, and KLF4, there are still no appropriate drugs to use. For NANOG and ALDH1 inhibitors, such as Amcasertib and Disulfiram 48 , 49 , our preliminary data showed that their anti-tumor effect in HNSCC was not as good as MYCi975.…”

Section: Discussionmentioning

confidence: 89%

Pharmacological inhibition of MYC to mitigate chemoresistance in preclinical models of squamous cell carcinoma

Liu,

Qin,

Mao

et al. 2024

Theranostics

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Rationale: Cisplatin-based chemotherapy is the first-line treatment for late-stage head and neck squamous cell carcinoma (HNSCC). However, resistance to cisplatin has become a major obstacle for effective therapy. Cancer stem cells (CSCs) are critical for tumor initiation, growth, metastasis, and chemoresistance. How to effectively eliminate CSCs and overcome chemoresistance remains a key challenge. Herein, we confirmed that MYC plays critical roles in chemoresistance, and explored targeting MYC to overcome cisplatin resistance in preclinical models. Methods: The roles of MYC in HNSCC cisplatin resistance and cancer stemness were tested in vitro and in vivo . The combined therapeutic efficiency of MYC targeting using the small molecule MYC inhibitor MYCi975 and cisplatin was assessed in a 4‑nitroquinoline 1-oxide-induced model and in a patient-derived xenograft model. Results: MYC was highly-expressed in cisplatin-resistant HNSCC. Targeting MYC using MYCi975 eliminated CSCs, prevented metastasis, and overcame cisplatin resistance. MYCi975 also induced tumor cell-intrinsic immune responses, and promoted CD8 + T cell infiltration. Mechanistically, MYCi975 induced the DNA damage response and activated the cGAS-STING-IRF3 signaling pathway to increase CD8 + T cell-recruiting chemokines. Conclusions: Our findings suggested that targeting MYC might eliminate CSCs, prevent metastasis, and activate antitumor immunity to overcome cisplatin resistance in HNSCC.

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Section: Discussionmentioning

confidence: 89%

Pharmacological inhibition of MYC to mitigate chemoresistance in preclinical models of squamous cell carcinoma

Liu,

Qin,

Mao

et al. 2024

Theranostics

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“…Ccl5 has been shown to be increased in the cortex of aging mice, which may be related to various aging processes [24] . Hmgb1 is involved in the function of muscle cells and participates in the appearance of aging phenotypes [25] , [26] . In contrast, Calm1|Sell between Natural killer cell and CD4 follicular helper T cell, Calm1|Sell between CD4 helper T cell 1 and CD4 follicular helper T cell, Calm1|Sell between B cell and CD4 follicular helper T cell, Calm1|Sell between Neutrophil and CD4 follicular helper T cell and Calm1|Sell between Monocyte and CD4 follicular helper T cell had the smallest MS values (<−0.4) ( Fig.…”

Section: Resultsmentioning

confidence: 99%

A global view of altered ligand-receptor interactions in bone marrow aging based on single-cell sequencing

Chen,

Yao

et al. 2024

Computational and Structural Biotechnology Journal

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PKR deficiency delays vascular aging via inhibiting GSDMD-mediated endothelial cell hyperactivation

Cited by 2 publications

References 27 publications

Pharmacological inhibition of MYC to mitigate chemoresistance in preclinical models of squamous cell carcinoma

Pharmacological inhibition of MYC to mitigate chemoresistance in preclinical models of squamous cell carcinoma

A global view of altered ligand-receptor interactions in bone marrow aging based on single-cell sequencing

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