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We are analyzing https://link.springer.com/article/10.1186/s12885-018-4504-5.

Title:
Resveratrol induces autophagy-dependent apoptosis in HL-60 cells | BMC Cancer
Description:
Background All known mechanisms of apoptosis induced by resveratrol act through cell cycle arrest and changes in mitochondrial membrane potential. It is currently unknown whether resveratrol-induced apoptosis is associated with other physiological processes, such as autophagy. Methods Apoptosis-related markers involved in the intrinsic and extrinsic apoptotic pathways, and autophagic markers were detected by using western blotting and immunofluorescence. Mitochondrial membrane potential was assayed by flow cytometry. Pharmaceutical or genetic inhibition of autophagy involved were carried by 3- methyladenine or knockdown of autophagy-related (Atg) genes by siRNA. Differences between two values were tested by Student’s unpaired t test. Results We show that resveratrol-induced apoptosis occurs through both the intrinsic and extrinsic apoptotic pathways. Mitochondrial membrane potential and apoptosis-related markers, such as an increased Bax/Bcl-2 ratio, and cleaved forms of caspase-8 and caspase-3, arise following resveratrol addition. Moreover, we find that resveratrol increases both the levels of microtubule-associated protein 1 light chain 3-II and the number of autophagosomes, and further demonstrate that resveratrol-induced autophagy depends on the LKB1-AMPK-mTOR pathway. We next reveal that some apoptosis-related markers induced by resveratrol are further attenuated by the inhibition of autophagy with 3-methyladenine or knockdown of autophagy-related (Atg) genes by siRNA. Conclusions These results suggest that resveratrol induced apoptotic cell death of HL-60 cells depends on the autophagy activated through both the LKB1-AMPK and PI3K/AKT-regulated mTOR signaling pathways.
Website Age:
28 years and 1 months (reg. 1997-05-29).

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  • Science
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What CMS is link.springer.com built with?

Custom-built

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🌠 Phenomenal Traffic: 5M - 10M visitors per month


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Keywords {🔍}

rsv, cells, cell, apoptosis, autophagy, article, death, caspase, pubmed, scholar, treated, google, resveratrol, cas, data, fig, induces, analysis, cancer, pathway, control, treatment, induced, western, inhibition, mtor, blot, times, pathways, time, intrinsic, results, analyzed, study, expression, rsvinduced, viability, concentrations, mitochondrial, involved, increased, protein, activation, experiments, activity, zhang, manner, extrinsic, apoptotic, cleaved,

Topics {✒️}

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Schema {🗺️}

WebPage:
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         headline:Resveratrol induces autophagy-dependent apoptosis in HL-60 cells
         description:All known mechanisms of apoptosis induced by resveratrol act through cell cycle arrest and changes in mitochondrial membrane potential. It is currently unknown whether resveratrol-induced apoptosis is associated with other physiological processes, such as autophagy. Apoptosis-related markers involved in the intrinsic and extrinsic apoptotic pathways, and autophagic markers were detected by using western blotting and immunofluorescence. Mitochondrial membrane potential was assayed by flow cytometry. Pharmaceutical or genetic inhibition of autophagy involved were carried by 3- methyladenine or knockdown of autophagy-related (Atg) genes by siRNA. Differences between two values were tested by Student’s unpaired t test. We show that resveratrol-induced apoptosis occurs through both the intrinsic and extrinsic apoptotic pathways. Mitochondrial membrane potential and apoptosis-related markers, such as an increased Bax/Bcl-2 ratio, and cleaved forms of caspase-8 and caspase-3, arise following resveratrol addition. Moreover, we find that resveratrol increases both the levels of microtubule-associated protein 1 light chain 3-II and the number of autophagosomes, and further demonstrate that resveratrol-induced autophagy depends on the LKB1-AMPK-mTOR pathway. We next reveal that some apoptosis-related markers induced by resveratrol are further attenuated by the inhibition of autophagy with 3-methyladenine or knockdown of autophagy-related (Atg) genes by siRNA. These results suggest that resveratrol induced apoptotic cell death of HL-60 cells depends on the autophagy activated through both the LKB1-AMPK and PI3K/AKT-regulated mTOR signaling pathways.
         datePublished:2018-05-22T00:00:00Z
         dateModified:2018-05-22T00:00:00Z
         pageStart:1
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         license:http://creativecommons.org/publicdomain/zero/1.0/
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         keywords:
            Resveratrol
            Apoptosis
            Autophagy
            Cell death
            PI3K-Akt
            AMPK-mTOR
            HL-60
            Cancer Research
            Oncology
            Surgical Oncology
            Health Promotion and Disease Prevention
            Biomedicine
            general
            Medicine/Public Health
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      headline:Resveratrol induces autophagy-dependent apoptosis in HL-60 cells
      description:All known mechanisms of apoptosis induced by resveratrol act through cell cycle arrest and changes in mitochondrial membrane potential. It is currently unknown whether resveratrol-induced apoptosis is associated with other physiological processes, such as autophagy. Apoptosis-related markers involved in the intrinsic and extrinsic apoptotic pathways, and autophagic markers were detected by using western blotting and immunofluorescence. Mitochondrial membrane potential was assayed by flow cytometry. Pharmaceutical or genetic inhibition of autophagy involved were carried by 3- methyladenine or knockdown of autophagy-related (Atg) genes by siRNA. Differences between two values were tested by Student’s unpaired t test. We show that resveratrol-induced apoptosis occurs through both the intrinsic and extrinsic apoptotic pathways. Mitochondrial membrane potential and apoptosis-related markers, such as an increased Bax/Bcl-2 ratio, and cleaved forms of caspase-8 and caspase-3, arise following resveratrol addition. Moreover, we find that resveratrol increases both the levels of microtubule-associated protein 1 light chain 3-II and the number of autophagosomes, and further demonstrate that resveratrol-induced autophagy depends on the LKB1-AMPK-mTOR pathway. We next reveal that some apoptosis-related markers induced by resveratrol are further attenuated by the inhibition of autophagy with 3-methyladenine or knockdown of autophagy-related (Atg) genes by siRNA. These results suggest that resveratrol induced apoptotic cell death of HL-60 cells depends on the autophagy activated through both the LKB1-AMPK and PI3K/AKT-regulated mTOR signaling pathways.
      datePublished:2018-05-22T00:00:00Z
      dateModified:2018-05-22T00:00:00Z
      pageStart:1
      pageEnd:10
      license:http://creativecommons.org/publicdomain/zero/1.0/
      sameAs:https://doi.org/10.1186/s12885-018-4504-5
      keywords:
         Resveratrol
         Apoptosis
         Autophagy
         Cell death
         PI3K-Akt
         AMPK-mTOR
         HL-60
         Cancer Research
         Oncology
         Surgical Oncology
         Health Promotion and Disease Prevention
         Biomedicine
         general
         Medicine/Public Health
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                     name:Open Laboratory for Tumor Molecular Biology/Department of Biochemistry/The Key Laboratory of Molecular Biology for High Cancer Incidence Coastal Chaoshan Area, Shantou University Medical College, Shantou, China
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            type:Person
            name:Jen-Fu Chiu
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                  name:Shantou University Medical College
                  address:
                     name:Open Laboratory for Tumor Molecular Biology/Department of Biochemistry/The Key Laboratory of Molecular Biology for High Cancer Incidence Coastal Chaoshan Area, Shantou University Medical College, Shantou, China
                     type:PostalAddress
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            name:Jing Liu
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                  name:Shantou University Medical College
                  address:
                     name:Cheung Kong Scholar Laboratory, Shantou University Medical College, Shantou, China
                     type:PostalAddress
                  type:Organization
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            name:Yan Deng
            affiliation:
                  name:Shantou University Medical College
                  address:
                     name:Open Laboratory for Tumor Molecular Biology/Department of Biochemistry/The Key Laboratory of Molecular Biology for High Cancer Incidence Coastal Chaoshan Area, Shantou University Medical College, Shantou, China
                     type:PostalAddress
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                     type:PostalAddress
                  type:Organization
            type:Person
            name:Cheng Xu
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                  name:Shantou University Medical College
                  address:
                     name:Open Laboratory for Tumor Molecular Biology/Department of Biochemistry/The Key Laboratory of Molecular Biology for High Cancer Incidence Coastal Chaoshan Area, Shantou University Medical College, Shantou, China
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Jun Zhang
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                  name:Shantou University Medical College
                  address:
                     name:Open Laboratory for Tumor Molecular Biology/Department of Biochemistry/The Key Laboratory of Molecular Biology for High Cancer Incidence Coastal Chaoshan Area, Shantou University Medical College, Shantou, China
                     type:PostalAddress
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            type:Person
            name:Guanwu Li
            url:http://orcid.org/0000-0003-3133-4460
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                  name:Shantou University Medical College
                  address:
                     name:Open Laboratory for Tumor Molecular Biology/Department of Biochemistry/The Key Laboratory of Molecular Biology for High Cancer Incidence Coastal Chaoshan Area, Shantou University Medical College, Shantou, China
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         name:Open Laboratory for Tumor Molecular Biology/Department of Biochemistry/The Key Laboratory of Molecular Biology for High Cancer Incidence Coastal Chaoshan Area, Shantou University Medical College, Shantou, China
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      address:
         name:Open Laboratory for Tumor Molecular Biology/Department of Biochemistry/The Key Laboratory of Molecular Biology for High Cancer Incidence Coastal Chaoshan Area, Shantou University Medical College, Shantou, China
         type:PostalAddress
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      name:Yingying Fan
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            name:Shantou University Medical College
            address:
               name:Open Laboratory for Tumor Molecular Biology/Department of Biochemistry/The Key Laboratory of Molecular Biology for High Cancer Incidence Coastal Chaoshan Area, Shantou University Medical College, Shantou, China
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      name:Jen-Fu Chiu
      affiliation:
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            address:
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            address:
               name:Cheung Kong Scholar Laboratory, Shantou University Medical College, Shantou, China
               type:PostalAddress
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      name:Yan Deng
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            name:Shantou University Medical College
            address:
               name:Open Laboratory for Tumor Molecular Biology/Department of Biochemistry/The Key Laboratory of Molecular Biology for High Cancer Incidence Coastal Chaoshan Area, Shantou University Medical College, Shantou, China
               type:PostalAddress
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            name:Shantou University Medical College
            address:
               name:Open Laboratory for Tumor Molecular Biology/Department of Biochemistry/The Key Laboratory of Molecular Biology for High Cancer Incidence Coastal Chaoshan Area, Shantou University Medical College, Shantou, China
               type:PostalAddress
            type:Organization
      name:Jun Zhang
      affiliation:
            name:Shantou University Medical College
            address:
               name:Open Laboratory for Tumor Molecular Biology/Department of Biochemistry/The Key Laboratory of Molecular Biology for High Cancer Incidence Coastal Chaoshan Area, Shantou University Medical College, Shantou, China
               type:PostalAddress
            type:Organization
      name:Guanwu Li
      url:http://orcid.org/0000-0003-3133-4460
      affiliation:
            name:Shantou University Medical College
            address:
               name:Open Laboratory for Tumor Molecular Biology/Department of Biochemistry/The Key Laboratory of Molecular Biology for High Cancer Incidence Coastal Chaoshan Area, Shantou University Medical College, Shantou, China
               type:PostalAddress
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      email:[email protected]
PostalAddress:
      name:Open Laboratory for Tumor Molecular Biology/Department of Biochemistry/The Key Laboratory of Molecular Biology for High Cancer Incidence Coastal Chaoshan Area, Shantou University Medical College, Shantou, China
      name:Open Laboratory for Tumor Molecular Biology/Department of Biochemistry/The Key Laboratory of Molecular Biology for High Cancer Incidence Coastal Chaoshan Area, Shantou University Medical College, Shantou, China
      name:Cheung Kong Scholar Laboratory, Shantou University Medical College, Shantou, China
      name:Open Laboratory for Tumor Molecular Biology/Department of Biochemistry/The Key Laboratory of Molecular Biology for High Cancer Incidence Coastal Chaoshan Area, Shantou University Medical College, Shantou, China
      name:Respiratory Department, The first Affiliated Hospital of Shantou University Medical College, Shantou, China
      name:Open Laboratory for Tumor Molecular Biology/Department of Biochemistry/The Key Laboratory of Molecular Biology for High Cancer Incidence Coastal Chaoshan Area, Shantou University Medical College, Shantou, China
      name:Open Laboratory for Tumor Molecular Biology/Department of Biochemistry/The Key Laboratory of Molecular Biology for High Cancer Incidence Coastal Chaoshan Area, Shantou University Medical College, Shantou, China
      name:Open Laboratory for Tumor Molecular Biology/Department of Biochemistry/The Key Laboratory of Molecular Biology for High Cancer Incidence Coastal Chaoshan Area, Shantou University Medical College, Shantou, China

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