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  1. Article ; Online: Correction: DJ-1 promotes epithelial-to-mesenchymal transition via enhancing FGF9 expression in colorectal cancer.

    Li, Longhao / Zhang, Chundong / Li, Yi / Zhang, Ying / Lei, Yunlong

    Biology open

    2023  Volume 12, Issue 1

    Language English
    Publishing date 2023-01-12
    Publishing country England
    Document type Published Erratum
    ZDB-ID 2632264-X
    ISSN 2046-6390 ; 2046-6390
    ISSN (online) 2046-6390
    ISSN 2046-6390
    DOI 10.1242/bio.059782
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: The ROCK-ezrin signaling pathway mediates LPS-induced cytokine production in pulmonary alveolar epithelial cells.

    Ding, Ning / Li, Pibao / Li, Huiqing / Lei, Yunlong / Zhang, Zengzhen

    Cell communication and signaling : CCS

    2022  Volume 20, Issue 1, Page(s) 65

    Abstract: Background: Ezrin/radixin/moesin (ERM) proteins are members of the protein 4.1 superfamily and function as linkers that connect the actin cytoskeleton to the plasma membrane of cells. ERM also play critical role in the Lipopolysaccharide (LPS)-induced ... ...

    Abstract Background: Ezrin/radixin/moesin (ERM) proteins are members of the protein 4.1 superfamily and function as linkers that connect the actin cytoskeleton to the plasma membrane of cells. ERM also play critical role in the Lipopolysaccharide (LPS)-induced inflammatory response. However, the signaling mechanisms involved in this process remain unclear. In this study, we aimed to investigate the potential role of the rho-associated coiled-coil containing protein kinase (ROCK) pathway in LPS-induced ezrin phosphorylation and cytokine production in pulmonary alveolar epithelial cells.
    Methods: Cultured A549 and HPAEpiC cells were treated with LPS. The expression and localization of ezrin in A549 and HPAEpiC cells were then analyzed by western blotting and immunoflurescence. Activation of RhoA/ROCK was assessed by western blotting and RhoA activity assays. The interaction of ezrin with Syk and myeloid differentiation factor 88 (MyD88)/IL-1R-associated kinase 1 (IRAK-1) was investigated by co-immunoprecipitation. The activation of nuclear factor-κB (NF-κB) and mitogen-activated protein kinase (MAPK) was measured with electrophoretic mobility shift assays and by western blotting. ELISA and western blotting were performed to detect the levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and high mobility group box 1 protein (HMGB1) release into the culture supernatant, and cellular HMGB1 levels.
    Results: LPS induced ezrin phosphorylation in a concentration- and time-dependent manner. The blockade of RhoA/ROCK inhibited LPS-induced ezrin phosphorylation and its translocation from the cytoplasm to the cell membrane. Co-immunoprecipitation assays further revealed that ezrin associated with Syk constitutively, but only associated with MyD88/IRAK-1 upon LPS challenge. Moreover, LPS-induced p38 and nuclear NF-κB activation was found to be ezrin dependent. The suppression of ezrin by siRNA or the blockade of ROCK activation with Y-27632 reduced the production of TNF-α, IL-1β, and HMGB1 in response to LPS.
    Conclusions: Our findings reveal a novel regulatory mechanism involving ezrin in the LPS-induced production of pro-inflammatory cytokines, and highlight the importance of the RhoA/ROCK-ezrin/Syk-MyD88/IRAK1 axis. Data presented in this manuscript provide novel insights into the signaling pathways activated in pulmonary alveolar epithelial cells by LPS. Video Abstract.
    MeSH term(s) Alveolar Epithelial Cells/metabolism ; Cytokines/metabolism ; Cytoskeletal Proteins ; HMGB1 Protein/metabolism ; Lipopolysaccharides/pharmacology ; Myeloid Differentiation Factor 88/metabolism ; NF-kappa B/metabolism ; Signal Transduction ; Tumor Necrosis Factor-alpha/metabolism
    Chemical Substances Cytokines ; Cytoskeletal Proteins ; HMGB1 Protein ; Lipopolysaccharides ; Myeloid Differentiation Factor 88 ; NF-kappa B ; Tumor Necrosis Factor-alpha ; ezrin
    Language English
    Publishing date 2022-05-12
    Publishing country England
    Document type Journal Article ; Video-Audio Media ; Research Support, Non-U.S. Gov't
    ZDB-ID 2126315-2
    ISSN 1478-811X ; 1478-811X
    ISSN (online) 1478-811X
    ISSN 1478-811X
    DOI 10.1186/s12964-022-00879-3
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: rRNA-Derived Small RNA rsRNA-28S Regulates the Chemoresistance of Prostate Cancer Cells by Targeting PTGIS.

    Qiao, Deqian / Liu, Yiling / Lei, Yunlong / Zhang, Chundong / Bu, Youquan / Tang, Yishu / Zhang, Ying

    Frontiers in bioscience (Landmark edition)

    2023  Volume 28, Issue 5, Page(s) 102

    Abstract: Background: rRNA-derived small RNAs (rsRNAs) represent a novel class of small non-coding RNAs (sncRNAs), produced by the specific cleavage of rRNAs; however, their roles in tumor development are unclear. In the present study, we explored the effect of a ...

    Abstract Background: rRNA-derived small RNAs (rsRNAs) represent a novel class of small non-coding RNAs (sncRNAs), produced by the specific cleavage of rRNAs; however, their roles in tumor development are unclear. In the present study, we explored the effect of a kind of rsRNA-28S, which originates from 28S rRNA, on the chemoresistance of prostate cancer cells and the mechanisms underlying its effect.
    Methods: Quantitative reverse transcription PCR (RT-PCR) was performed to quantify rsRNA-28S levels in serum samples taken from prostate cancer patients. DU-145R cells, which are resistant to both paclitaxel and docetaxel, were generated from parental DU-145 cells. Northern blot was conducted to detect cellular rsRNA-28S levels following drug treatments. To verify the effect of rsRNAs-28S on chemoresistance, antisense oligonucleotides were utilized to block rsRNA-28S functions, and a series of assays were further performed, such as cell viability, cell proliferation, colony formation and tumor sphere formation. The target gene of rsRNA-28S was explored using dual-luciferase reporter gene assay.
    Results: The rsRNA-28S level was reduced in the serum samples of patients who received chemotherapy compared to that of patients who did not. Furthermore, the rsRNA-28S level was remarkably declined in DU-145R cells, and drug treatments decreased the levels of rsRNA-28S in DU-145 and DU-145R cells. Moreover, rsRNA-28S inhibition enhanced the chemoresistance of prostate cancer cells as well as their cancer stem cell characteristics. Mechanistically, the prostaglandin I2 synthase (
    Conclusions: Our findings indicate that rsRNA-28S attenuates prostate cancer cell chemoresistance by downregulating its target gene
    MeSH term(s) Male ; Humans ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Drug Resistance, Neoplasm/genetics ; Prostatic Neoplasms/drug therapy ; Prostatic Neoplasms/genetics ; Prostatic Neoplasms/pathology ; Docetaxel/pharmacology ; Docetaxel/therapeutic use ; Cell Proliferation/genetics ; RNA, Messenger ; Cell Line, Tumor ; Gene Expression Regulation, Neoplastic ; Cytochrome P-450 Enzyme System/genetics ; Cytochrome P-450 Enzyme System/metabolism ; Cytochrome P-450 Enzyme System/pharmacology
    Chemical Substances MicroRNAs ; Docetaxel (15H5577CQD) ; RNA, Messenger ; PTGIS protein, human (EC 5.3.99.4) ; Cytochrome P-450 Enzyme System (9035-51-2)
    Language English
    Publishing date 2023-05-31
    Publishing country Singapore
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2704569-9
    ISSN 2768-6698 ; 2768-6698
    ISSN (online) 2768-6698
    ISSN 2768-6698
    DOI 10.31083/j.fbl2805102
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: The expression of kappa-opioid receptor promotes the migration of breast cancer cells in vitro.

    Li, Huiqing / Ma, Zhenzhen / Lei, Yunlong

    BMC anesthesiology

    2021  Volume 21, Issue 1, Page(s) 210

    Abstract: Background: Opioid receptors are implicated in cell proliferation and cancer migration. However, the effects and underlying mechanisms of opioid receptor κ (OPRK1) in breast cancer remain unknown.: Methods: Small interfering RNA (siRNAs) was used to ... ...

    Abstract Background: Opioid receptors are implicated in cell proliferation and cancer migration. However, the effects and underlying mechanisms of opioid receptor κ (OPRK1) in breast cancer remain unknown.
    Methods: Small interfering RNA (siRNAs) was used to knockdown the expression of OPRK1. Western blot was used to determine the protein expression and reverse transcription-quantitative PCR (RT-qPCR) determined the genes transcription. Cell viability was detected by MTT assay and cell death rates were determined by Annexin V/PI and flow cytometry. Cell migration and invasion were detected by wound healing analysis and transwell assay, respectively.
    Results: Our research demonstrated that OPRK1 was overexpressed in breast cancer cells compared with the normal human mammary epithelial cells. OPRK1 knockdown could inhibited cell viability and migration in cancer cells, accompanied with the decreased proteins and genes expression of N-cadherin, Snail, MMP2 and Vimentin, while the E-cadherin expression was increased. Additionally, OPRK1 knockdown also promoted PI3K/AKT signaling inactivation. Activation of AKT reversed the OPRK1 knockdown-induced cell viability inhibition and migration suppression, while inhibition of AKT reduced cell viability and promoted cell death.
    Conclusions: Our findings illustrated the role of OPRK1 played on promoting migration in vitro, and we also provided the therapeutic research of OPRK1 knockdown combined with AKT inhibition.
    MeSH term(s) Breast Neoplasms/pathology ; Cell Line, Tumor ; Cell Movement ; Cell Survival ; Female ; Gene Silencing ; Humans ; Phosphatidylinositol 3-Kinases/genetics ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins c-akt/genetics ; Proto-Oncogene Proteins c-akt/metabolism ; RNA, Small Interfering ; Receptors, Opioid, kappa/genetics ; Receptors, Opioid, kappa/metabolism ; Signal Transduction
    Chemical Substances OPRK1 protein, human ; RNA, Small Interfering ; Receptors, Opioid, kappa ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
    Language English
    Publishing date 2021-08-30
    Publishing country England
    Document type Journal Article
    ISSN 1471-2253
    ISSN (online) 1471-2253
    DOI 10.1186/s12871-021-01429-z
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: The Effect of Sediment Supply on Pool‐Riffle Morphology

    Lei, Yunlong / Hassan, Marwan A. / Viparelli, Enrica / Chartrand, Shawn M. / An, Chenge / Fu, Xudong / Hu, Chunhong

    Water Resources Research. 2023 Nov., v. 59, no. 11 p.e2023WR035983-

    2023  

    Abstract: Downstream width variations can generate pool‐riffle morphology under experimental conditions, in numerical simulations and natural river channels. The present understanding of how pool‐riffle morphology varies with sediment supply and caliber, however, ... ...

    Abstract Downstream width variations can generate pool‐riffle morphology under experimental conditions, in numerical simulations and natural river channels. The present understanding of how pool‐riffle morphology varies with sediment supply and caliber, however, is insufficient due to the limited range of sediment supply rates explored in previous experiments and the little attention paid to sand supply and sediment size distribution in the laboratory and in the field. We present a model of river morphodynamics that can account for the spatial variability of channel width, and we validate the model with experimental data. Model validation shows how this one‐dimensional model can capture pool‐riffle formation, growth, and equilibration with errors that are comparable with those of other 1D models of river morphodynamics. We then apply the validated model to study the effects of sediment supply rate and caliber on pool‐riffle morphology. Model results show that pool‐riffle morphology is resilient to the range of tested sediment supply (i.e., five‐fold the sediment amount, 41‐fold the sand amount and coarsening the gravel supply). Bed and water surface slopes are sensitive to all types of change of sediment supply, whereas the sensitivity of bed surface sediment grain size varies with the type of change. These findings support prior research emphasizing the role of downstream width variations for the development/maintenance of pool‐riffle morphology and can help in the restoration and recovery of pool‐riffle gravel‐bed rivers.
    Keywords gravel ; model validation ; models ; research ; rivers ; sand ; water
    Language English
    Dates of publication 2023-11
    Publishing place John Wiley & Sons, Ltd
    Document type Article ; Online
    Note JOURNAL ARTICLE
    ZDB-ID 5564-5
    ISSN 1944-7973 ; 0043-1397
    ISSN (online) 1944-7973
    ISSN 0043-1397
    DOI 10.1029/2023WR035983
    Database NAL-Catalogue (AGRICOLA)

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  6. Article ; Online: Transfer RNA-derived small RNAs (tsRNAs): Versatile regulators in cancer.

    Xu, Dandan / Qiao, Deqian / Lei, Yunlong / Zhang, Chundong / Bu, Youquan / Zhang, Ying

    Cancer letters

    2022  Volume 546, Page(s) 215842

    Abstract: tRNA-derived small RNAs (tsRNAs) represent a novel class of regulatory small non-coding RNAs (sncRNAs), produced by the specific cleavage of transfer RNAs (tRNAs). In recent years, pilot studies one after the other have uncovered the critical roles of ... ...

    Abstract tRNA-derived small RNAs (tsRNAs) represent a novel class of regulatory small non-coding RNAs (sncRNAs), produced by the specific cleavage of transfer RNAs (tRNAs). In recent years, pilot studies one after the other have uncovered the critical roles of tsRNAs in various fundamental biological processes as well as in the development of human diseases including cancer. Based on the newly updated hallmarks of cancer, we provide a comprehensive review regarding the dysregulation, functional implications and complicated molecular mechanisms of tsRNAs in cancer. In addition, the potential technical challenges and future prospects in the fields of tsRNA research are discussed in this review.
    MeSH term(s) Humans ; Neoplasms ; RNA, Small Untranslated ; RNA, Transfer
    Chemical Substances RNA, Small Untranslated ; RNA, Transfer (9014-25-9)
    Language English
    Publishing date 2022-08-11
    Publishing country Ireland
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 195674-7
    ISSN 1872-7980 ; 0304-3835
    ISSN (online) 1872-7980
    ISSN 0304-3835
    DOI 10.1016/j.canlet.2022.215842
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article: Ciclopirox Olamine Induces Proliferation Inhibition and Protective Autophagy in Hepatocellular Carcinoma.

    Wan, Xinyan / Xiang, Junqi / Fan, Hui / Jiang, Ying / Lu, Yiting / Zhang, Chundong / Zhang, Ying / Chen, Quanmei / Lei, Yunlong

    Pharmaceuticals (Basel, Switzerland)

    2023  Volume 16, Issue 1

    Abstract: Hepatocellular carcinoma is one of the most common fatal malignancies worldwide. Thus far, the hepatocellular carcinoma prognosis has been bleak due to deficiencies in the identification and diagnosis of early hepatocellular carcinoma. Ciclopirox olamine ...

    Abstract Hepatocellular carcinoma is one of the most common fatal malignancies worldwide. Thus far, the hepatocellular carcinoma prognosis has been bleak due to deficiencies in the identification and diagnosis of early hepatocellular carcinoma. Ciclopirox olamine (CPX) is a synthetic antifungal agent and has been considered as an anti-cancer candidate drug recently, though the detailed mechanisms related to its anti-cancer effect in hepatocellular carcinoma have not yet been revealed. Here, we found that CPX could inhibit proliferation in HCC cells but not in intrahepatic cholangiocarcinoma cells by arresting the cell cycle. Moreover, the anti-cancer effects of CPX in HCC cells were also attributed to CPX-triggered ROS accumulation and DJ-1 downregulation. Additionally, CPX could promote complete autophagic flux, which alleviated the anti-cancer effect of CPX in HCC cells, whereas the ROS scavenger (NAC) would attenuate CPX-induced protective autophagy. Interestingly, CPX could also induce glycogen clustering in HCC cells. Altogether, this study provides a new insight into the detailed molecular mechanisms of CPX as an anti-cancer therapy and a strategy for treating hepatocellular carcinoma.
    Language English
    Publishing date 2023-01-12
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2193542-7
    ISSN 1424-8247
    ISSN 1424-8247
    DOI 10.3390/ph16010113
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article: DJ-1 promotes epithelial-to-mesenchymal transition via enhancing FGF9 expression in colorectal cancer.

    Li, Longhao / Zhang, Chundong / Li, Yi / Zhang, Ying / Lei, Yunlong

    Biology open

    2020  Volume 9, Issue 5

    Abstract: Tumor metastasis is the main contributor to high recurrence and mortality in colorectal cancer (CRC). In a previous study, we found that DJ-1 plays an important role in CRC metastasis, and is the main target in Ciclopirox olamine (CPX)-treated CRC. ... ...

    Abstract Tumor metastasis is the main contributor to high recurrence and mortality in colorectal cancer (CRC). In a previous study, we found that DJ-1 plays an important role in CRC metastasis, and is the main target in Ciclopirox olamine (CPX)-treated CRC. However, the mechanism underlying DJ-1-induced CRC metastasis remains elusive. In the present study, our results showed that DJ-1 could activate Wnt signaling resulting in enhanced invasive potential and epithelial-to-mesenchymal transition (EMT) in CRC cells. RNA-seq and bioinformatics analysis reveals that the DJ-1/Wnt signaling pathway may promote CRC cells' EMT by regulating fibroblast growth factor 9 (FGF9) expression. Molecular validation showed that expression of FGF9 was upregulated by the DJ-1/Wnt signaling pathway and decreasing FGF9-expression impeded DJ-1-induced CRC invasive ability and EMT, suggesting that FGF9 is involved in DJ-1-enhanced CRC metastasis. In addition, we show that FGF9 was overexpressed in CRC human specimens and was significantly associated with tumor differentiation. High FGF9 expression was correlated with worse overall survival, and a correlation exhibited between FGF9 and EMT markers (E-cadherin and Vimentin) in CRC samples. Together, our results determined that FGF9 was involved in DJ-1-induced invasion and EMT in CRC cells, and may represent a promising therapeutic candidate for CRC anti-metastatic strategies.
    MeSH term(s) Cell Line, Tumor ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/metabolism ; Colorectal Neoplasms/mortality ; Colorectal Neoplasms/pathology ; Epithelial-Mesenchymal Transition/genetics ; Fibroblast Growth Factor 9/genetics ; Fibroblast Growth Factor 9/metabolism ; Gene Expression Regulation, Neoplastic ; Humans ; Immunohistochemistry ; Prognosis ; Protein Deglycase DJ-1/genetics ; Protein Deglycase DJ-1/metabolism ; Wnt Signaling Pathway
    Chemical Substances FGF9 protein, human ; Fibroblast Growth Factor 9 ; PARK7 protein, human (EC 3.1.2.-) ; Protein Deglycase DJ-1 (EC 3.1.2.-)
    Language English
    Publishing date 2020-05-19
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2632264-X
    ISSN 2046-6390
    ISSN 2046-6390
    DOI 10.1242/bio.051680
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Tubeimoside-I sensitizes colorectal cancer cells to chemotherapy by inducing ROS-mediated impaired autophagolysosomes accumulation.

    Yan, Jianghong / Dou, Xiaoyun / Zhou, Jing / Xiong, Yuanfeng / Mo, Ling / Li, Longhao / Lei, Yunlong

    Journal of experimental & clinical cancer research : CR

    2019  Volume 38, Issue 1, Page(s) 353

    Abstract: Background: Tubeimoside-I (TBM), a plant-derived bioactive compound, shows antitumor activity in different tumors and can enhance the efficacy of chemotherapeutic agents. However, the detail mechanism underlying remains to be elucidated.: Methods: ... ...

    Abstract Background: Tubeimoside-I (TBM), a plant-derived bioactive compound, shows antitumor activity in different tumors and can enhance the efficacy of chemotherapeutic agents. However, the detail mechanism underlying remains to be elucidated.
    Methods: The cytotoxic potential of TBM towards CRC cells was examined by CCK8 assay, colony formation, LDH release assay, flow cytometry method and Western blots. The ROS levels, autophagy, apoptosis, chemosensitivity to 5-FU or DOX, etc. were determined between control and TBM-treated CRC cells.
    Results: In this study, we found that TBM could inhibit proliferation and induce apoptosis in colorectal cancer (CRC) cells. Intriguingly, TBM treatment could either promote autophagy initiation by ROS-induced AMPK activation, or block autophagy flux through inhibiting lysosomal hydrolytic enzymes, which leaded to massive impaired autophagylysosomes accumulation. Administration of autophagy initiation inhibitor (3-MA or selective ablation of autophagy related proteins) relieves TBM-induced CRC suppression, while combination use of autophagy flux inhibitor chloroquine (CQ) slightly augments TBM-induced cell death, suggesting that impaired autophagylysosomes accumulation contributes to TBM-induced growth inhibition in CRC cells. Notably, as an autophagy flux inhibitor, TBM works synergistically with 5-fluorouracil (5-FU) or doxorubicin (DOX) in CRC suppression.
    Conclusion: Together, our study provides new insights regarding the anti-tumor activity of TBM against CRC, and established potential applications of TBM for CRC combination therapies in clinic.
    MeSH term(s) Antineoplastic Agents/pharmacology ; Apoptosis/drug effects ; Autophagy/drug effects ; Cell Line, Tumor ; Cell Survival/drug effects ; Drug Resistance, Neoplasm/drug effects ; Drug Synergism ; Drugs, Chinese Herbal/pharmacology ; Fluorouracil/pharmacology ; Humans ; Lysosomes/metabolism ; Phagosomes/metabolism ; Proteolysis/drug effects ; Reactive Oxygen Species/metabolism ; Saponins/pharmacology ; Signal Transduction/drug effects ; Triterpenes/pharmacology
    Chemical Substances Antineoplastic Agents ; Drugs, Chinese Herbal ; Reactive Oxygen Species ; Saponins ; Triterpenes ; tubeimoside I (102040-03-9) ; Fluorouracil (U3P01618RT)
    Language English
    Publishing date 2019-08-14
    Publishing country England
    Document type Journal Article
    ZDB-ID 803138-1
    ISSN 1756-9966 ; 0392-9078
    ISSN (online) 1756-9966
    ISSN 0392-9078
    DOI 10.1186/s13046-019-1355-0
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article: Targeting Metabolic-Redox Circuits for Cancer Therapy.

    Wang, Kui / Jiang, Jingwen / Lei, Yunlong / Zhou, Shengtao / Wei, Yuquan / Huang, Canhua

    Trends in biochemical sciences

    2019  Volume 44, Issue 5, Page(s) 401–414

    Abstract: Metabolic alterations and elevated levels of reactive oxygen species (ROS) are two characteristics of cancer. The metabolic patterns of cancer cells are elaborately reprogrammed to fulfill the high biomass demands of rapid propagation. ROS, the ... ...

    Abstract Metabolic alterations and elevated levels of reactive oxygen species (ROS) are two characteristics of cancer. The metabolic patterns of cancer cells are elaborately reprogrammed to fulfill the high biomass demands of rapid propagation. ROS, the byproducts of metabolic processes, are accumulated in cancer cells partially due to metabolic abnormalities or oncogenic mutations. To prevent oxidative damage, cancer cells can orchestrate metabolic adaptation to maintain reduction-oxidation (redox) balance by producing reducing equivalents. ROS, acting as second messengers, can in turn manipulate metabolic pathways by directly or indirectly affecting the function of metabolic enzymes. In this review we discuss how cancer cell metabolism and redox signaling are intertwined, with an emphasis on the perspective of targeting metabolic-redox circuits for cancer therapy.
    MeSH term(s) Animals ; Humans ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Neoplasms/pathology ; Oxidation-Reduction ; Reactive Oxygen Species/metabolism
    Chemical Substances Reactive Oxygen Species
    Language English
    Publishing date 2019-01-21
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 194216-5
    ISSN 1362-4326 ; 0968-0004 ; 0376-5067
    ISSN (online) 1362-4326
    ISSN 0968-0004 ; 0376-5067
    DOI 10.1016/j.tibs.2019.01.001
    Database MEDical Literature Analysis and Retrieval System OnLINE

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