Psoralidin induced reactive oxygen species (ROS)-dependent DNA damage and protective autophagy mediated by NOX4 in breast cancer cells

Ren, Guowen; Luo, Weiwei; Sun, Wenyue; Niu, Yanan; Ma, Dik‐Lung; Leung, Chung‐Hang; Wang, Ying; Lu, Jin‐Jian; Chen, Xiuping

doi:10.1016/j.phymed.2016.05.008

Cited by 41 publications

(21 citation statements)

References 33 publications

(36 reference statements)

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“…2B, exposure to 20 µM SH-4-54 markedly reduced the levels of ROS in the K562/G cells (P=0.872 vs. K562; P=0.01 vs. K562/G). It is well established that ROS can induce DNA damage, including DNA DSBs, and is generally recognized as an inducer of resistance mutation; γ-H2AX is frequently observed in regions of histone lesions resulting from ROS damage and may be used to quantify DSBs (20). The present study showed that higher levels of γ-H2AX were detected in the K562/G cells than in the K562 cells, which suggested that higher levels of ROS and secondary DNA damage were present in the K562/G cells.…”

Section: Ros Accumulation Contributes To Enhanced Levels Of Dnamentioning

confidence: 99%

Persistent STAT5-mediated ROS production and involvement of aberrant p53 apoptotic signaling in the resistance of chronic myeloid leukemia to imatinib

et al. 2017

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The persistent activation of signal transducer and activator of transcription 5 (STAT5) may principally be attributed to breakpoint cluster region (BCR)-Abelson murine leukemia viral oncogene homolog 1 (ABL1), and have multi-faceted effects in the development of chronic myeloid leukemia (CML). The p53 protein network regulates important mechanisms in DNA damage repair, cell cycle regulation/checkpoints, and cell senescence and apoptosis, as demonstrated by its ability to positively regulate the expression of various pro-apoptotic genes, including B-cell lymphoma-2 (Bcl-2) and Bcl-2-associated X protein (Bax). In the present study, it was observed that the mRNA levels of STAT5A and STAT5B were upregulated in patients with imatinib-resistant CML and in the imatinib-resistant K562/G CML cell line. In addition, increased expression of STAT5 was observed in the BCR-ABL1 mutation group, compared with that in the non-BCR-ABL1 mutation group, regardless of patient imatinib resistance state. Elevated levels of reactive oxygen species (ROS) and DNA double-strand breaks were identified in K562/G cells using flow cytometric and phosphorylated H2AX (γ-H2AX) foci immunofluorescence assays, respectively, compared with the imatinib-sensitive K562 cells. The levels of intracellular ROS and γ-H2AX were decreased by the ROS scavenger (N-acetylcysteine), and ROS levels were also markedly reduced by STAT5 inhibitor (SH-4-54). In addition, imatinib significantly inhibited the proliferation of K562 and K562/G cells, with half maximal inhibitory concentration values of 0.17±0.07 and 14.78±0.43 µM, respectively, and the levels of apoptosis were significantly different between K562 and K562/G cells following treatment with imatinib. The mRNA and protein levels of STAT5 and mouse double minute 2 homolog (MDM2) were upregulated, whereas those of Bax were downregulated in K562/G cells, as determined using western blot analysis. Additionally, although the two cell lines exhibited relatively low protein expression levels of p53, lower levels of p53 and TPp53BP1 transcripts were detected in the K562/G cells. Taken together, these findings suggest that the resistance of CML to the tyrosine kinase inhibitor, imatinib, may be associated with persistent STAT5-mediated ROS production, and the abnormality of the p53 pathway.

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Section: Ros Accumulation Contributes To Enhanced Levels Of Dnamentioning

confidence: 99%

Persistent STAT5-mediated ROS production and involvement of aberrant p53 apoptotic signaling in the resistance of chronic myeloid leukemia to imatinib

et al. 2017

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“…Two flavanoids compounds, isobavachalcone (IBC) and bacachinin (BCN), are believed to inhibit the process of A β 42 aggregation and suppress A β 42‐induced toxicity in human neuroblastoma cells, providing a potential treatment for Alzheimer's disease (Chen et al, ). Accumulating evidence suggests that P. corylifolia L. is a potential medicine against cancer, Parkinson's disease, infertility, depression and cocaine addiction (Ren et al, ; Mazzio et al, ; Yang et al, ; Zhao et al, ).…”

Section: Introductionmentioning

confidence: 99%

Qualitative analysis of Psoraleae Fructus by HPLC‐DAD/TOF‐MS fingerprint and quantitative analysis of multiple components by single marker

Luan

Shen

Liu

et al. 2017

Biomedical Chromatography

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A variety of bioactive substances may account for the recognized efficacy and wide clinical application of Psoraleae Fructus in China. A high-performance liquid chromatography-diode array detector (HPLC-DAD) fingerprint method was developed to present the comprehensive phytochemical profile of the crude drug. Thirteen major compounds were separated and identified by HPLC coupled with time-of-flight mass spectrometry (HPLC/TOF-MS), namely psoralenoside (PO), isopsoralenoside (IPO), psoralen (PS), isopsoralen (IPS), neobavaisoflavone (NBF), bavachin (BC), corylin (CN), bavachromene (BCM), psoralidin (PD), isobavachalcone (IBC), bacachinin (BCN), corylifol A (CA) and bakuchiol (BK). Then quantitative analysis of multiple components by single marker (QAMS) was applied in content determination of PO, IPO, PS, IPS, BC, IBC, BCN, CA and BK, with NBF as the internal standard. The calculation results indicated no significant difference from the traditional external standard method (p > 0.05, RSD < 2.62%), suggesting that QAMS is a reliable and convenient method for content determination of multiple chemical compositions, especially when there is a shortage of reference substances. In conclusion, simultaneous qualitative and quantitative analysis of Psoraleae Fructus may be fulfilled through the newly proposed method of QAMS combined with HPLC-DAD/TOF-MS fingerprint.

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“…It can serve as a second messenger to regulate signal transduction, related to cell proliferation, differentiation, apoptosis, and autophagy (Djavaheri-Mergny et al, 2007;Liu et al, 2009). Numerous studies have shown that ROS can attack the DNA, causing DNA damage, such as DNA strand breaks, DNA site mutations, DNA double-stranded aberrations, proto-oncogenes, and tumor suppressor gene mutations (Ren et al, 2016). The MAPK family is a group of serine/threonine kinases, including the extracellular signal-regulated kinase pathway, c-Jun N-terminal kinase pathway, and p38 MAPK pathway.…”

Section: Introductionmentioning

confidence: 99%

TEOA Inhibits Proliferation and Induces DNA Damage of Diffuse Large B-Cell Lymphoma Cells Through Activation of the ROS-Dependent p38 MAPK Signaling Pathway

Wang

et al. 2020

Front. Pharmacol.

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Diffuse large B-cell lymphoma (DLBCL) is the most common subtype of lymphoma, accounting for approximately 30% to 40% of non-Hodgkin's lymphomas (NHL). The administration of rituximab significantly improved the outcomes of DLBCL; however, the unavoidable development of resistance limits the long-term efficacy. Therefore, a new generation of less toxic drugs with higher chemotherapy response is required to prevent or reverse chemoresistance. TEOA is a pentacyclic triterpenoid compound isolated from the roots of Actinidia eriantha. Studies have confirmed that TEOA has significant cytotoxicity on gastrointestinal cancer cells. However, there are no relevant reports on DLBCL cells. In this study, we investigated the potential molecular mechanism of the anticancer activity of TEOA in DLBCL cells. The results demonstrated that TEOA inhibited proliferation and induced apoptosis in time-and dose-dependent manners. TEOA induced reactive oxygen species (ROS) generation, which was reversed by N-acetyl cysteine (NAC). TEOA induced DNA damage, increased the level of g-H2AX, and the phosphorylation of CHK1 and CHK2. In addition, TEOA induced the activation of the p38 MAPK pathway and pretreated with p38 inhibitor SB20358 or ROS scavenger could block TEOA-induced DNA damage. Taken together, these results suggest that ROS mediated activation of the p38 MAPK signal pathway plays an important role in initiating TEOA-induced DNA damage.

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Psoralidin induced reactive oxygen species (ROS)-dependent DNA damage and protective autophagy mediated by NOX4 in breast cancer cells

Cited by 41 publications

References 33 publications

Persistent STAT5-mediated ROS production and involvement of aberrant p53 apoptotic signaling in the resistance of chronic myeloid leukemia to imatinib

Persistent STAT5-mediated ROS production and involvement of aberrant p53 apoptotic signaling in the resistance of chronic myeloid leukemia to imatinib

Qualitative analysis of Psoraleae Fructus by HPLC‐DAD/TOF‐MS fingerprint and quantitative analysis of multiple components by single marker

TEOA Inhibits Proliferation and Induces DNA Damage of Diffuse Large B-Cell Lymphoma Cells Through Activation of the ROS-Dependent p38 MAPK Signaling Pathway

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