Caspase-3 knockout attenuates radiation-induced tumor repopulation via impairing the ATM/p53/Cox-2/PGE2 pathway in non-small cell lung cancer

Zhao, Minghui; Wang, Yiwei; Zhao, Yucui; He, Sijia; Zhao, Ruyi; Song, Yanwei; Cheng, Jin; Gong, Yanping; Xie, Jianzhu; Wang, Yulan; Hu, Binjie; Tian, Ling; Huang, Qian

doi:10.18632/aging.103984

Cited by 19 publications

(33 citation statements)

References 57 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Recent studies reported that radiation-induced dying cancer cells stimulate tumour cell proliferation mainly through caspase 3-mediated signalling (13,28,29), but few reports have described chemotherapy-induced tumour cell repopulation. To address whether tumour repopulation might be involved in the low efficacy of gemcitabine against BDC, we performed conditioned medium transfer experiments, which have been reported to reflect cell-cell interactions (17)(18)(19).…”

Section: Discussionmentioning

confidence: 99%

“…This signal transduction cascade activates the release of mitogens including Wingless (analogue Wnt), Decapentaplegic (a member of the β-transforming growth factor family) and NOTCH, thus inducing compensatory proliferation (7,11,12). Although there is limited research on the molecular mechanism of dying cellmediated cell proliferation in human cancer, a recent study reported that caspase-3-mediated ataxia telangiectasia mutated (ATM)/TP53/cyclo-oxygenase-2/prostaglandin E 2 signalling contributes to radiation-induced tumour repopulation in nonsmall cell lung cancer cells (13). It is therefore highly likely that the caspase-TP53 axis is a key player in tumour repopulation following chemoradiotherapy.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Exosomal p38 Mitogen-activated Protein Kinase Promotes Tumour Repopulation in TP53-mutated Bile Duct Cancer Cells

Osawa¹,

Matsuda²,

Sakata³

et al. 2022

Anticancer Res

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Exosomal p38 Mitogen-activated Protein Kinase Promotes Tumour Repopulation in TP53-mutated Bile Duct Cancer Cells

Osawa¹,

Matsuda²,

Sakata³

et al. 2022

Anticancer Res

View full text Add to dashboard Cite

“…IR-induced DSBs’ triggering of ATM-dependent activation of transcription factors NF-κB and STAT3 driving tumor growth, and late-phase exosome biosynthesis and release (after caspase-3 cleavage of the pore-forming protein DFNA) may contribute to maintaining the viability of neighboring cells and promote anastasis [ 408 ]. The important role of caspase-3 was demonstrated by the fact that caspase-3 knockout considerably reduced IR-induced tumor repopulation by decreasing endoG release from mitochondria to nuclei and impairing the ATM/p53/Cox2/PGF 2 pathway in non-small cell lung cancer [ 409 ].…”

Section: Ionizing Radiation (Ir) Effects Involving Mitochondriamentioning

confidence: 99%

“…The phenomenon of anastasis is because damaged cells seek and take other secondary metabolic pathways trying to ensure cell survival. After low-LET photon exposures, some cells succeed in escaping from apoptosis by fission and fusion of mitochondria to reconstitute healthy mitochondria from partially damaged, dysfunctional mitochondria [ 408 , 409 ].…”

Section: Ionizing Radiation (Ir) Effects Involving Mitochondriamentioning

confidence: 99%

Role of Mitochondria in Radiation Responses: Epigenetic, Metabolic, and Signaling Impacts

Averbeck

Rodriguez-Lafrasse

2021

IJMS

110

View full text Add to dashboard Cite

Until recently, radiation effects have been considered to be mainly due to nuclear DNA damage and their management by repair mechanisms. However, molecular biology studies reveal that the outcomes of exposures to ionizing radiation (IR) highly depend on activation and regulation through other molecular components of organelles that determine cell survival and proliferation capacities. As typical epigenetic-regulated organelles and central power stations of cells, mitochondria play an important pivotal role in those responses. They direct cellular metabolism, energy supply and homeostasis as well as radiation-induced signaling, cell death, and immunological responses. This review is focused on how energy, dose and quality of IR affect mitochondria-dependent epigenetic and functional control at the cellular and tissue level. Low-dose radiation effects on mitochondria appear to be associated with epigenetic and non-targeted effects involved in genomic instability and adaptive responses, whereas high-dose radiation effects (>1 Gy) concern therapeutic effects of radiation and long-term outcomes involving mitochondria-mediated innate and adaptive immune responses. Both effects depend on radiation quality. For example, the increased efficacy of high linear energy transfer particle radiotherapy, e.g., C-ion radiotherapy, relies on the reduction of anastasis, enhanced mitochondria-mediated apoptosis and immunogenic (antitumor) responses.

show abstract

“…This overexpression was mostly associated with DNA degradation in the promoter/exon 1 regions of the endonuclease genes [133], although EndoG is also able to participate in alternative splicing of DNase I mRNA [134]. Interestingly, the overexpression of EndoG is important for the development of tumor progression, and the silencing of the EndoG gene contributes to the suppression of the proliferation of tumor cells [135,136].…”

Section: Intracellular Dnasesmentioning

confidence: 99%

Role of Cell-Free DNA and Deoxyribonucleases in Tumor Progression

Alekseeva

Миронова

2021

IJMS

View full text Add to dashboard Cite

Many studies have reported an increase in the level of circulating cell-free DNA (cfDNA) in the blood of patients with cancer. cfDNA mainly comes from tumor cells and, therefore, carries features of its genomic profile. Moreover, tumor-derived cfDNA can act like oncoviruses, entering the cells of vulnerable organs, transforming them and forming metastatic nodes. Another source of cfDNA is immune cells, including neutrophils that generate neutrophil extracellular traps (NETs). Despite the potential eliminative effect of NETs on tumors, in some cases, their excessive generation provokes tumor growth as well as invasion. Considering both possible pathological contributions of cfDNA, as an agent of oncotransformation and the main component of NETs, the study of deoxyribonucleases (DNases) as anticancer and antimetastatic agents is important and promising. This review considers the pathological role of cfDNA in cancer development and the role of DNases as agents to prevent and/or prohibit tumor progression and the development of metastases.

show abstract

Caspase-3 knockout attenuates radiation-induced tumor repopulation via impairing the ATM/p53/Cox-2/PGE2 pathway in non-small cell lung cancer

Cited by 19 publications

References 57 publications

Exosomal p38 Mitogen-activated Protein Kinase Promotes Tumour Repopulation in TP53-mutated Bile Duct Cancer Cells

Exosomal p38 Mitogen-activated Protein Kinase Promotes Tumour Repopulation in TP53-mutated Bile Duct Cancer Cells

Role of Mitochondria in Radiation Responses: Epigenetic, Metabolic, and Signaling Impacts

Role of Cell-Free DNA and Deoxyribonucleases in Tumor Progression

Contact Info

Product

Resources

About