bims-rehoca Biomed News
on Redox homeostasis in cancer
Issue of 2021–12–19
fourteen papers selected by
Vittoria Raimondi, Veneto Institute of Oncology
  1. Glutathione-Responsive Chemodynamic Therapy of Manganese(III/IV) Cluster Nanoparticles Enhanced by Electrochemical Stimulation via Oxidative Stress Pathway.
  2. Moderate Static Magnet Fields Suppress Ovarian Cancer Metastasis via ROS-Mediated Oxidative Stress.
  3. Trichomonas vaginalis induces apoptosis via ROS and ER stress response through ER-mitochondria crosstalk in SiHa cells.
  4. The Feasibility Study of Plasma-activated Water as a Physical Therapy to Induce Apoptosis in Melanoma Cancer Cells In-vitro.
  5. Nanoparticles: A Promising Tool to Promote Reactive Oxygen Species in Cancer Therapy.
  6. Ethyl acetate extract of Clausena excavata induces growth inhibition of non-small-lung cancer, NCI-H460, cell line via apoptosis.
  7. Carnosic Acid Suppresses the Development of Oral Squamous Cell Carcinoma via Mitochondrial-Mediated Apoptosis.
  8. Crosstalk between anticancer drugs and mitochondrial functions.
  9. Ferroptosis: The Silver Lining of Cancer Therapy.
  10. Photoacoustic nanodroplets for oxygen enhanced photodynamic therapy of cancer.
  11. Evaluation of anticancer activity in vitro of a stable copper(I) complex with phosphine-peptide conjugate.
  12. Feedback regulation of antioxidant transcription factor NFE2L1 and immunostimulatory factor 41BBL mediates the crosstalk between oxidative stress and tumor immunity.
  13. Electrochemical measuring of reactive oxygen species levels in the blood to detect ratio of high-density neutrophils, suitable to alarm presence of cancer in suspicious cases.
  14. High-performance SOD mimetic enzyme Au@Ce for arresting cell cycle and proliferation of acute myeloid leukemia.
  1. Bioconjug Chem. 2021 Dec 14.
    Glutathione-Responsive Chemodynamic Therapy of Manganese(III/IV) Cluster Nanoparticles Enhanced by Electrochemical Stimulation via Oxidative Stress Pathway.
    Yang Chen, Ming Chen, Tianli Zhai, Han Zhou, Zhiguo Zhou, Xiaoming Liu, Shiping Yang, Hong Yang.
      Escalating the level of reactive oxygen species (ROS) in a tumor microenvironment is one of the effective strategies to improve the efficacy of anticancer therapy. In this work, manganese cluster nanoparticles (Mn12) encapsulated with heparin (Mn12-heparin) were developed as a chemodynamic therapeutic agent for cancer treatment by raising ROS levels in tumor cells via cascade reactions. The manganese cluster is a cluster of mixed valence (III/IV) with acetate as the ligand. The cluster is readily subject to reduction by glutathione (GSH) to release Mn(II), which reacts with H2O2 to generate hydroxyl radicals via a Fenton-like pathway. The generation of hydroxyl radicals could be enhanced by the stimulation of an external alternative electric field during which GSH acts as an electron mediator to enhance the release of Mn(II) from the cluster. The relatively high levels of both H2O2 and GSH and the acidic environment in tumor cells strengthen its specificity when the manganese cluster system is employed to suppress or eliminate tumors. Both in vitro and in vivo results suggest that, in addition to the cytotoxicity imposed by the raised ROS level due to the presence of Mn(II) species, the depletion of endogenous GSH leads indirectly to the inhibition of glutathione peroxidase 4 (GPX4), consequently raising the lipid peroxidation (LPO) level to cause ferroptosis. The apoptosis and ferroptosis jointly render the manganese-based agent potent efficacy with tumor-targeting specificity in antitumor treatment under electric stimulation.
    DOI:  https://doi.org/10.1021/acs.bioconjchem.1c00512
  2. Oxid Med Cell Longev. 2021 ;2021 7103345
    Moderate Static Magnet Fields Suppress Ovarian Cancer Metastasis via ROS-Mediated Oxidative Stress.
    Chao Song, Biao Yu, Junjun Wang, Xinmiao Ji, Lei Zhang, Xiaofei Tian, Xin Yu, Chuanlin Feng, Xinyu Wang, Xin Zhang.
      Metastasis is the leading cause of cancer patient death, which is closely correlated with reactive oxygen species (ROS) levels. It is well known that the effects of ROS on tumors are diverse, depending on ROS concentration and cell type. We found that ovarian cancer cells have significantly lower levels of ROS than normal ovarian cells. Moreover, increased ROS levels in ovarian cancer cells can substantially inhibit their migration and invasion ability. Furthermore, the results show that moderate static magnetic field (SMF) can inhibit ovarian cancer cell migration, invasion, and stemness in a ROS-dependent manner. RNA sequencing results confirm that SMFs increased the oxidative stress level and reduced the stemness of ovarian cancer cells. Consistently, the expressions of stemness-related genes were significantly decreased, including hyaluronan receptor (CD44), SRY-box transcription factor 2 (Sox2), and cell myc proto-oncogene protein (C-myc). Furthermore, moderate SMFs provided by a superconducting magnet and permanent magnet have good biosafety and can both inhibit ovarian cancer metastasis in mice. Therefore, our study demonstrates the effects of SMFs on oxidative stress and metastasis in the ovarian cancer cells, which reveals the potential of applying SMF as a physical method in cancer therapy in the future.
    DOI:  https://doi.org/10.1155/2021/7103345
  3. Parasit Vectors. 2021 Dec 11. 14(1): 603
    Trichomonas vaginalis induces apoptosis via ROS and ER stress response through ER-mitochondria crosstalk in SiHa cells.
    Fei Fei Gao, Juan-Hua Quan, Min A Lee, Wei Ye, Jae-Min Yuk, Guang-Ho Cha, In-Wook Choi, Young-Ha Lee.
       BACKGROUND: Trichomonas vaginalis causes lesions on the cervicovaginal mucosa in women; however, its pathogenesis remains unclear. We have investigated the involvement of the endoplasmic reticulum (ER) in the induction of apoptosis by T. vaginalis and its molecular mechanisms in human cervical cancer SiHa cells.
    METHODS: Apoptosis, reactive oxygen species (ROS) production, mitochondrial membrane potential (MMP), ER stress response and Bcl-2 family protein expression were evaluated using immunocytochemistry, flow cytometry, 5,5',6,6'-tetrachloro-1,1',3,3'-tetraethyl-imidacarbocyanine iodide dye staining and western blotting.
    RESULTS: Trichomonas vaginalis induced mitochondrial ROS production, apoptosis, the ER stress response and mitochondrial dysfunction, such as MMP depolarization and an imbalance in Bcl-2 family proteins, in SiHa cells in a parasite burden- and infection time-dependent manner. Pretreatment with N-acetyl cysteine (ROS scavenger) or 4-phenylbutyric acid (4-PBA; ER stress inhibitor) significantly alleviated apoptosis, mitochondrial ROS production, mitochondrial dysfunction and ER stress response in a dose-dependent manner. In addition, T. vaginalis induced the phosphorylation of apoptosis signal regulating kinase 1 (ASK1) and c-Jun N-terminal kinases (JNK) in SiHa cells, whereas 4-PBA or SP600125 (JNK inhibitor) pretreatment significantly attenuated ASK1/JNK phosphorylation, mitochondrial dysfunction, apoptosis and ER stress response in SiHa cells, in a dose-dependent manner. Furthermore, T. vaginalis excretory/secretory products also induced mitochondrial ROS production, apoptosis and the ER stress response in SiHa cells, in a time-dependent manner.
    CONCLUSIONS: Trichomonas vaginalis induces apoptosis through mitochondrial ROS and ER stress responses, and also promotes ER stress-mediated mitochondrial apoptosis via the IRE1/ASK1/JNK/Bcl-2 family protein pathways in SiHa cells. These data suggest that T. vaginalis-induced apoptosis is affected by ROS and ER stress response via ER-mitochondria crosstalk.
    Keywords:  Endoplasmic reticulum stress; Human cervical cancer SiHa cells; Mitochondrial apoptosis; Reactive oxygen species; Trichomonas vaginalis
    DOI:  https://doi.org/10.1186/s13071-021-05098-2
  4. Iran J Pharm Res. 2021 ;20(3): 337-350
    The Feasibility Study of Plasma-activated Water as a Physical Therapy to Induce Apoptosis in Melanoma Cancer Cells In-vitro.
    Hamed Mahdikia, Babak Shokri, Keivan Majidzadeh-A.
      Low-temperature plasma (LTP) has demonstrated great potential in biomedicine, especially in cancer therapy in-vivo and in-vitro. Plasma activated water (PAW) as an indirect plasma therapy is a significant source of reactive oxygen and nitrogen species (RONS) which play an important role in apoptosis induction in cancer cells. In this study, Helium (He) plasma jet operating in 0.75 W and 20 kHz as dissipated power and frequency, respectively, is used as the cold plasma source. The electrical, thermal, and spectroscopic properties of (He) plasma jet and pH as well as the conductivity and temperature of PAW samples, are investigated. The concentration of hydrogen peroxide (H2O2), nitrite (NO2 -) and nitrate (NO- 3), which are produced in water as long-lived anticancer RONS, was measured 471.6, 7.9 and 93.5 μM, respectively after 6 min of plasma treatment. Alamar Blue and flow cytometry assays were employed to investigate the B16F10 cancer metabolic activity and apoptosis. These data support that cold atmospheric plasma (CAP) can produce a certain concentration of anti-cancer agents in water and induce apoptosis in melanoma cancer cells due to RONSs via activating the caspase 3 pathway.
    Keywords:  Apoptosis; Melanoma; Plasma Gases; Reactive nitrogen species (RNS); Reactive oxygen species (ROS); Resazurin
    DOI:  https://doi.org/10.22037/ijpr.2021.114493.14882
  5. Curr Protein Pept Sci. 2021 Dec 09.
    Nanoparticles: A Promising Tool to Promote Reactive Oxygen Species in Cancer Therapy.
    Mahima Chauhan, Saurabh Shekhar, Bhavna Yadav, Vandana Garg, Rohit Dutt, Sonali, Rahul Pratap Singh.
      
    Keywords:  Cancer cell death; Cancer therapy; Drug delivery technology; Nanomedicines; Reactive Oxygen Species
    DOI:  https://doi.org/10.2174/1389203722666211210115819
  6. J Appl Biomed. 2021 Mar;19(1): 40-47
    Ethyl acetate extract of Clausena excavata induces growth inhibition of non-small-lung cancer, NCI-H460, cell line via apoptosis.
    Shaymaa Fadhel Abbas Albaayit, Mariam Ashfaq Khan, Rasedee Abdullah, Mohd Hezmee Mohd Noor.
       CONTEXT: Clausena excavata Burm. f is a plant used in folklore medicine for the treatment of various ailments in South East Asia. The plant parts contain chemical components that are cytotoxic to many cancer cells.
    OBJECTIVE: The study investigated the cytotoxic effects of ethyl acetate, methanol and chloroform C. excavata leaf extracts on the non-small-lung cancer, NCI-H460, cell line.
    METHODS: Based on the 3-(4,5-dimethylthiazol-2-yl)-2,5,-diphenyltetrazolium bromide (MTT) assay, among extracts, ethyl acetate C. excavata leaf extract (EACE) was the most potent anti-NCI-H460 cells, with IC50 value of 47.1 ± 6.1 μg/ml. The effects of EACE on NCI-H460 cells were also determined by clonogenic, 4', 6-diamidino-2-phenylindole (DAPI), and annexin-V-fluorescein isothiocyanate/propidium iodide-PI flow cytometric assays. Reactive oxygen species (ROS) production and apoptotic gene expressions was determined via flow cytometry and real-time quantitative PCR, respectively.
    RESULTS: EACE-treated NCI-H460 cells after 48 h underwent apoptosis as evident by loss of cell viability, cell shrinkage, and chromatin condensation. The results also showed EACE mediated increase in ROS production by the NCI-H460 cells. After 48 h treatment, EACE increased the pro-apoptotic BAX and decreased the anti-apoptotic Bcl-2, Survivin and c-Myc gene expressions.
    CONCLUSIONS: EACE is a potential anti-lung cancer by increasing cancer cell ROS production and apoptosis.
    Keywords:  Apoptosis; Cytotoxicity; ROS; Survivin
    DOI:  https://doi.org/10.32725/jab.2021.007
  7. Front Oncol. 2021 ;11 760861
    Carnosic Acid Suppresses the Development of Oral Squamous Cell Carcinoma via Mitochondrial-Mediated Apoptosis.
    Fenghe Min, Xin Liu, Yuan Li, Mingyuan Dong, Yidi Qu, Weiwei Liu.
      Oral squamous cell carcinoma (OSCC) predominantly consists of squamous cells and is the tumor with the highest incidence of the head and neck. Carnosic acid (CA), a natural monomer drug obtained from rosemary and salvia, shows various pharmacological effects, including of tumor development. This study aimed to assess for an effect of CA on the development of OSCC and the underlying mechanisms. In CAL27 and SCC9 cells, CA inhibited cell proliferation and migration, increased intracellular levels of reactive oxygen species (ROS) and Ca2+, decreased the mitochondrial membrane potential (MMP), and promoted apoptosis. In CAL27- and SCC9-xenotransplanted BALB/c nude mice, CA inhibited the tumor growth without affecting the body weight and tissue morphology. CA upregulated Bax, Bad, cleaved Caspase-3 and -9 levels, and the cleaved PARP1/PARP1 ratio but downregulated Bcl-2 in CA-treated OSCC cells and OSCC cells-xenotransplanted BALB/c nude mice. These results indicate that CA suppresses OSCC at least via the mitochondrial apoptotic pathway and offers this natural compound as a potential therapeutic against OSCC.
    Keywords:  apoptosis; carnosic acid; mitochondria; oral squamous cell carcinoma; reactive oxygen species
    DOI:  https://doi.org/10.3389/fonc.2021.760861
  8. Curr Res Pharmacol Drug Discov. 2021 ;2 100047
    Crosstalk between anticancer drugs and mitochondrial functions.
    Kuleshwar Sahu, Urvashi Langeh, Charan Singh, Arti Singh.
      Chemotherapy is an important component of cancer treatment, which has side effects like vomiting, peripheral neuropathy, and numerous organ toxicity but the most significant outcomes of chemotherapy are cognitive impairment, which is mainly referred to as chemobrain or CICI (chemotherapy-induced cognitive impairment). It is characterized by difficulty with language, concentrating, processing speed, learning, and memory, as it affects the hippocampus areas of the brain. Mitochondrial dysfunction and oxidative stress are one of the major mechanisms causing chemobrain. The generation of reactive oxygen species (byproducts of oxidative phosphorylation) mainly occurs in mitochondria that play a prominent role in the induction of oxidative stress. The homeostasis of ROS in the mitochondria is maintained by mitochondrial antioxidant mechanism via enzymes like catalase, glutathione, and superoxide dismutase. Lungs and breast cancer are the two most common types of cancer, which are the most leading cancers in the world with about 4.18 million cases. In this review we exposed the current knowledge regarding chemotherapy-induced oxidative stress and mitochondrial dysfunction to cause cognitive impairment.We especially focused on the antineoplastic agent (ADRIAMYCIN, CYCLOPHOSPHAMIDE), platinum group agent CISPLATIN, antimetabolite agents (METHOTREXATE), and nitrogen mustard agent (CARMUSTINE) which increase oxidative stress and inflammatory markers in the PNS (peripheral nervous system) as well as the central nervous system. We also highlight the behavioural and functional changes in the brain.
    Keywords:  Chemobrain; Chemotherapy; Cognitive impairment; Mitochondrial dysfunction; Oxidative stress; Reactive oxygen species
    DOI:  https://doi.org/10.1016/j.crphar.2021.100047
  9. Front Cell Dev Biol. 2021 ;9 765859
    Ferroptosis: The Silver Lining of Cancer Therapy.
    Zhengming Tang, Zhijie Huang, Yisheng Huang, Yuanxin Chen, Mingshu Huang, Hongyu Liu, Q Adam Ye, Jianjiang Zhao, Bo Jia.
      Regulatory cell death has been a major focus area of cancer therapy research to improve conventional clinical cancer treatment (e.g. chemotherapy and radiotherapy). Ferroptosis, a novel form of regulated cell death mediated by iron-dependent lipid peroxidation, has been receiving increasing attention since its discovery in 2012. Owing to the highly iron-dependent physiological properties of cancer cells, targeting ferroptosis is a promising approach in cancer therapy. In this review, we summarised the characteristics of ferroptotic cells, associated mechanisms of ferroptosis occurrence and regulation and application of the ferroptotic pathway in cancer therapy, including the use of ferroptosis in combination with other therapeutic modalities. In addition, we presented the challenges of using ferroptosis in cancer therapy and future perspectives that may provide a basis for further research.
    Keywords:  cancer therapy; ferroptosis; lipid peroxidation; reactive oxygen species; regulatory cell death
    DOI:  https://doi.org/10.3389/fcell.2021.765859
  10. Photoacoustics. 2022 Mar;25 100306
    Photoacoustic nanodroplets for oxygen enhanced photodynamic therapy of cancer.
    Marvin Xavierselvan, Jason Cook, Jeanne Duong, Nashielli Diaz, Kimberly Homan, Srivalleesha Mallidi.
      Photodynamic therapy (PDT) is a well-known cancer therapy that utilizes light to excite a photosensitizer and generate cytotoxic reactive oxygen species (ROS). The efficacy of PDT primarily depends on the photosensitizer and oxygen concentration in the tumor. Hypoxia in solid tumors promotes treatment resistance, resulting in poor PDT outcomes. Hence, there is a need to combat hypoxia while delivering sufficient photosensitizer to the tumor for ROS generation. Here we showcase our unique theranostic perfluorocarbon nanodroplets as a triple agent carrier for oxygen, photosensitizer, and indocyanine green that enables light triggered spatiotemporal delivery of oxygen to the tumors. We evaluated the characteristics of the nanodroplets and validated their ability to deliver oxygen via photoacoustic monitoring of blood oxygen saturation and subsequent PDT efficacy in a murine subcutaneous tumor model. The imaging results were validated with an oxygen sensing probe, which showed a 9.1 fold increase in oxygen content inside the tumor, following systemic administration of the nanodroplets. These results were also confirmed with immunofluorescence. In vivo studies showed that nanodroplets held higher rates of treatment efficacy than a clinically available benzoporphyrin derivative formulation. Histological analysis showed higher necrotic area within the tumor with perfluoropentane nanodroplets. Overall, the photoacoustic nanodroplets can significantly enhance image-guided PDT and has demonstrated substantial potential as a valid theranostic option for patient-specific photodynamic therapy-based treatments.
    Keywords:  1O2, singlet oxygen; BPD, benzoporphyrin derivative; DLS, dynamic light scattering; DPPC, 1,2-dipalmitoyl-sn-glycero-3-phosphocholine; DSPE-mPEG, 1,2-distearoyl-sn-glycero-3-phosphoethanolamine-N-[methoxy(polyethylene glycol)-2000]; H&E, hematoxylin and eosin; HbT, total hemoglobin; Hypoxia; ICG, indocyanine green; IF, immunofluorescence; Image guided PDT; MTT, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide; NIR, near infrared radiation; PA, photoacoustic; PBS, phosphate buffered saline; PDT, photodynamic therapy; PFC, perfluorocarbon; PFP, perfluoropentane; PS, photosensitizer; Perfluorocarbon nanodroplets; Photoacoustic imaging; Photodynamic therapy; ROS, reactive oxygen species; SOSG, singlet oxygen sensor green; StO2, oxygen saturation; TBAI, tertbutylammonium iodide; pO2, partial pressure of oxygen
    DOI:  https://doi.org/10.1016/j.pacs.2021.100306
  11. Sci Rep. 2021 Dec 14. 11(1): 23943
    Evaluation of anticancer activity in vitro of a stable copper(I) complex with phosphine-peptide conjugate.
    Urszula K Komarnicka, Barbara Pucelik, Daria Wojtala, Monika K Lesiów, Grażyna Stochel, Agnieszka Kyzioł.
      [CuI(2,9-dimethyl-1,10-phenanthroline)P(p-OCH3-Ph)2CH2SarcosineGlycine] (1-MPSG), highly stable in physiological media phosphino copper(I) complex-is proposed herein as a viable alternative to anticancer platinum-based drugs. It is noteworthy that, 1-MPSG significantly and selectively reduced cell viability in a 3D spheroidal model of human lung adenocarcinoma (A549), in comparison with non-cancerous HaCaT cells. Confocal microscopy and an ICP-MS analysis showed that 1-MPSG effectively accumulates inside A549 cells with colocalization in mitochondria and nuclei. A precise cytometric analysis revealed a predominance of apoptosis over the other types of cell death. In the case of HaCaT cells, the overall cytotoxicity was significantly lower, indicating the selective activity of 1-MPSG towards cancer cells. Apoptosis also manifested itself in a decrease in mitochondrial membrane potential along with the activation of caspases-3/9. Moreover, the caspase inhibitor (Z-VAD-FMK) pretreatment led to decreased level of apoptosis (more pronouncedly in A549 cells than in non-cancerous HaCaT cells) and further validated the caspases dependence in 1-MPSG-induced apoptosis. Furthermore, the 1-MPSG complex presumably induces the changes in the cell cycle leading to G2/M phase arrest in a dose-dependent manner. It was also observed that the 1-MPSG mediated intracellular ROS alterations in A549 and HaCaT cells. These results, proved by fluorescence spectroscopy, and flow cytometry, suggest that investigated Cu(I) compound may trigger apoptosis also through ROS generation.
    DOI:  https://doi.org/10.1038/s41598-021-03352-2
  12. Mol Immunol. 2021 Dec 11. pii: S0161-5890(21)00344-8. [Epub ahead of print]141 265-272
    Feedback regulation of antioxidant transcription factor NFE2L1 and immunostimulatory factor 41BBL mediates the crosstalk between oxidative stress and tumor immunity.
    Lu Qiu, Haoming Ning, Yaqian Zhu, Qiufang Yang, Lulu Liu, Lei Luo, Yanfeng Gao, Yadi Xing.
      Targeting the immune checkpoint to inhibit tumor immune escape, which is one of the fundamental causes of cancer, has become an important strategy for cancer treatment. The molecular mechanism of tumor immune escape involved in the process of spontaneous hepatocellular carcinoma after specifically knocking out NFE2L1, the core regulator of redox homeostasis, in the mouse liver is still unclear. Transcriptome data showed that the immunostimulatory TNFSF9/41BBL was significantly reduced in NFE2L1 knockdown hepatocarcinoma HepG2 cells, and this suggests that 41BBL may be an oxidative stress-responsive immune checkpoint. The results of the promoter activity experiment showed that NFE2L1 can promote 41BBL gene transcription activation through the ARE element in the promoter region. In addition, cell biology experiments have found that overexpression of 41BBL can inhibit cell proliferation and promote senescence. Importantly, reactive oxygen species in cells significantly increased after overexpression of 41BBL, whereas NFE2L1 was inhibited, indicating that 41BBL has the effect of feedback regulating oxidative stress in cells. In conclusion, in this study, the transcriptional activation effect of NFE2L1 on 41BBL and the feedback inhibition relationship of 41BBL on NFE2L1 was clarified. The NFE2L1/41BBL axis might be an important pathway that mediates the crosstalk between oxidative stress and the tumor immune response.
    Keywords:  Hepatocellular carcinoma/HCC; Immune checkpoint; NFE2L1/Nrf1; Oxidative stress; Reactive oxygen species/ROS; TNFSF9/41BBL
    DOI:  https://doi.org/10.1016/j.molimm.2021.12.001
  13. J Pharm Biomed Anal. 2021 Nov 29. pii: S0731-7085(21)00599-9. [Epub ahead of print]209 114488
    Electrochemical measuring of reactive oxygen species levels in the blood to detect ratio of high-density neutrophils, suitable to alarm presence of cancer in suspicious cases.
    Zohreh Sadat Miripour, Mina Aminifar, Mohammad Esmaeil Akbari, Fereshteh Abbasvandi, Seyyed Hossein Miraghaie, Parisa Hoseinpour, Mohammad Reza Javadi, Najmeh Dabbagh, Leily Mohajerzadeh, Maryam Kazemi Aghdam, Shahin Shamsian, Hassan Sanati, Mohammad Abdolahad.
      Here for the first time, a real-time electrochemical assay on unprocessed blood was designed to detect the presence of cancer in patients. The system has been based on the recently approved pathway, which indicates that the abundance of immature and mature low-density neutrophils (LDNs) with reduced ROS production in peripheral blood is increased with the presence of active cancer tumors. Reduced ROS/H2O2 released from LDNs play the main role in determining the ROS/H2O2 levels of peripheral blood. In contrast, HDNs with increased levels of released ROS/H2O2 have higher concentrations than LDNs in normal cases. Hence, the reduced level of ROS species in peripheral blood recorded by our carbon nanostructure decorated sensor in less than 30 seconds showed a great pre-warning about the presence of non-treated cancer in patients with suspicious mass who have been sent for further evaluations.
    Keywords:  Electrochemical assay; Immature and mature neutrophils; Low-density neutrophils; Non-treated cancer; Reactive oxygen species
    DOI:  https://doi.org/10.1016/j.jpba.2021.114488
  14. Bioact Mater. 2022 Apr;10 117-130
    High-performance SOD mimetic enzyme Au@Ce for arresting cell cycle and proliferation of acute myeloid leukemia.
    Yuxiang Sun, Xin Liu, Lei Wang, Li Xu, Kunliang Liu, Lei Xu, Fangfang Shi, Yu Zhang, Ning Gu, Fei Xiong.
      SOD-like activity of CeO2 nanoparticles (Ce NPs) is driven by Ce3+/Ce4+, high oxidative stress can oxidize Ce3+ to reduce the ratio of Ce3+/Ce4+, inactivating the SOD activity of Ce NPs. Herein, we found Au@Ce NPs, assembled by Au NPs and Ce NPs, exhibited high-performance of SOD mimetic enzyme activity even upon the oxidation of H2O2. Ce NPs supported by nano-Au can acquire the electrons from Au NPs through the enhanced localized surface plasmon resonance (LSPR), maintaining the stability of Ce3+/Ce4+ and SOD-like activity. Meanwhile, Au@Ce NPs retained the peroxidase function and catalase function. As a result, Au@Ce NPs effectively scavenged O2•- and the derived ROS in AML cells, which are the important signaling source that drives AML cell proliferation and accelerates cell cycle progression. When HL-60 cells were treated by Au@Ce NPs, the removal of endogenous ROS signal significantly arrested cell cycle at G1 phase and suppressed the cell proliferation by blocking the mitogen-activated protein kinases (MAPKs) signaling and the Akt/Cyclin D1 cell cycle signaling. Importantly, this treatment strategy showed therapeutic effect for subcutaneous transplantation of AML model as well as a satisfactory result in diminishing the leukocyte infiltration of liver and spleen particularly. Thus, assembled Au@Ce NPs show the high-performance SOD-like activity, promising the potential in treating AML and regulating abnormal ROS in other diseases safely and efficiently.
    Keywords:  Acute myeloid leukemia; Au nanoparticles; CeO2 nanoparticles; Reactive oxygen species; Superoxide dismutase
    DOI:  https://doi.org/10.1016/j.bioactmat.2021.08.012
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