Mechanisms of cancer cell death induction by triptolide: A comprehensive overview

Feng, Ke; Li, Xiaojiang; Bai, Yuzhuo; Zhang, Dawei; Tian, Lin

doi:10.1016/j.heliyon.2024.e24335

Cited by 5 publications

(2 citation statements)

References 147 publications

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“…The largest increase was exhibited by ERCC3 (excision repair 3 TFIIH core complex helicase subunit) in T (∆COORD = 34) and Θ (∆COORD = 64), and TAF1L (TATA-box binding protein associated factor 1 like) in Φ (∆COORD = 60). Expression coordination of ERCC3, also known as xeroderma-pigmentosum B (XPB) [89], also increased in Φ (∆COORD = 32). In contrast, GTF2I (general transcription factor IIi) in T (∆COORD = −44), GTF2H4 (general transcription factor IIH subunit 4) in Φ (∆COORD = −46), and TAF6 (TATA-box binding protein associated factor 6) in Θ (∆COORD = −44) exhibited the largest decrease.…”

Section: Additional Measures Of Transcriptomic Alterationsmentioning

confidence: 99%

Papillary Thyroid Cancer Remodels the Genetic Information Processing Pathways

Iacobas,

Iacobas

2024

Genes

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The genetic causes of the differentiated, highly treatable, and mostly non-fatal papillary thyroid cancer (PTC) are not yet fully understood. The mostly accepted PTC etiology blames the altered sequence or/and expression level of certain biomarker genes. However, tumor heterogeneity and the patient’s unique set of favoring factors question the fit-for-all gene biomarkers. Publicly accessible gene expression profiles of the cancer nodule and the surrounding normal tissue from a surgically removed PTC tumor were re-analyzed to determine the cancer-induced alterations of the genomic fabrics responsible for major functional pathways. Tumor data were compared with those of standard papillary and anaplastic thyroid cancer cell lines. We found that PTC regulated numerous genes associated with DNA replication, repair, and transcription. Results further indicated that changes of the gene networking in functional pathways and the homeostatic control of transcript abundances also had major contributions to the PTC phenotype occurrence. The purpose to proliferate and invade the entire gland may explain the substantial transcriptomic differences we detected between the cells of the cancer nodule and those spread in homo-cellular cultures (where they need only to survive). In conclusion, the PTC etiology should include the complex molecular mechanisms involved in the remodeling of the genetic information processing pathways.

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Section: Additional Measures Of Transcriptomic Alterationsmentioning

confidence: 99%

Papillary Thyroid Cancer Remodels the Genetic Information Processing Pathways

Iacobas,

Iacobas

2024

Genes

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“…Expression coordination of ERCC3, a.k.a. xeroderma-pigmentosum B (XPB) [80], increased also in Φ (ΔCOORD = 32). In contrast, GTF2I (general transcription factor IIi) in T (ΔCOORD = -44), GTF2H4 (general transcription factor IIH subunit 4) in Φ (ΔCOORD = -46) and TAF6 (TATA-box binding protein associated factor 6) in Θ (ΔCOORD = -44) exhibited the largest decrease.…”

Section: Additional Measures Of Transcriptomic Alterationsmentioning

confidence: 99%

Papillary Thyroid Cancer Remodels the Genomic Fabrics of DNA Replication, Repair and Transcription

Iacobas,

Iacobas

2024

Preprint

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The genetic causes of the differentiated, highly treatable and mostly non-fatal papillary thyroid cancer (PTC) are not yet fully known. The widely accepted PTC etiology blames altered sequence or/and expression level of certain biomarker genes. However, our previous studies found that the PTC biomarkers played significantly lower roles than the personalized PTC Gene Master Regulators. Our publicly accessible gene expression data from the cancer nodule and the surrounding normal tissue of surgically removed PTC tumor were re-analyzed to determine the transcriptomic effects on the genomic fabrics responsible for the DNA replication, repair and transcription. Tumor results were compared to the gene expression profiles of the papillary (BCPAP) and the anaplastic (8505C) human thyroid cancer cell lines. The analyses were carried out from the Genomic Fabric Paradigm (GFP) perspective that provides the most theoretically possible comprehensive characterization of the transcriptome and its alterations in disease. The study indicated that, in addition to regulating numerous genes, changes in the homeostatic control of transcript abundances and remodeling of the gene networks had major contributions to the PTC occurrence, resilience and proliferation. Therefore, the molecular mechanisms responsible for gene expression control and inter-coordination should also be considered when designing personalized anti-cancer gene therapies.

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Triptolide Promotes Ferroptosis in Cervical Cancer Cell via NRF2/xCT/GPX4

Feng,

Wu,

Zhu

et al. 2024

Phytotherapy Research

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Cervical cancer (CC) is a serious risk to women's health; it is necessary to explore less toxic and more effective therapies to cure CC. Triptolide (Tri) is the principal active constituent found in “Tripterygium Wilford,” has been shown to have antitumor effects. This study set up to demonstrate whether Tri is capable of inducing ferroptosis in CC cells and its potential mechanism. In vitro, Tri was used to treat CC cells, and lipid peroxidation levels in CC cells were detected by flow cytometry, immunofluorescence, and other experiments; the molecular mechanism of Tri treatment of CC was explored by western blot; moreover, the regulatory effects of Tri on the NRF2/GPX4/xCT axis were verified by overexpressing NRF2 in reverse. In vivo, CC cells tumor‐bearing mice were constructed to observe the effect of Tri treatment on tumor growth. In vitro, we have demonstrated that Tri prevents the growth and migration of CC cells. Further investigation revealed that Tri substantially enhances ferroptosis in CC cells by increasing lipid peroxidation accumulation. Mechanically, Tri significantly reduced the expression of NRF2, leading to a corresponding repression of the NRF2 downstream targets GPX4 and xCT. Moreover, overexpressing of NRF2 effectively reversed the impact of Tri on ferroptosis in CC cells. Additionally, animal experiments indicted that Tri markedly inhibited tumor size in nude mice by inhibiting the NRF2/GPX4/xCT axis. Tri exerts antitumor effects by triggering ferroptosis in CC cells through the NRF2/GPX4/xCT axis.

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Mechanisms of cancer cell death induction by triptolide: A comprehensive overview

Cited by 5 publications

References 147 publications

Papillary Thyroid Cancer Remodels the Genetic Information Processing Pathways

Papillary Thyroid Cancer Remodels the Genetic Information Processing Pathways

Papillary Thyroid Cancer Remodels the Genomic Fabrics of DNA Replication, Repair and Transcription

Triptolide Promotes Ferroptosis in Cervical Cancer Cell via NRF2/xCT/GPX4

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