Autophagy inhibition promotes paclitaxel-induced apoptosis in cancer cells

Paclitaxel has been demonstrated to be an effective mitotic inhibitor and apoptosis inducer to treat aggressive malignancies. In this paper, we have provided a line of evidence that promotion of apoptotic cell death by paclitaxel was accompanied with induction of autophagy in A549 cells. Paclitaxel...

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Published in	Cancer letters Vol. 307; no. 2; pp. 141 - 148
Main Authors	Xi, Guangmin, Hu, Xiaoyan, Wu, Baolin, Jiang, Hanming, Young, Charles Y.F., Pang, Yingxin, Yuan, Huiqing
Format	Journal Article
Language	English
Published	Ireland Elsevier Ireland Ltd 28.08.2011 Elsevier Limited
Subjects	Antibiotics Antineoplastic Agents, Phytogenic Antineoplastic Agents, Phytogenic - pharmacology Apoptosis Apoptosis - drug effects Autophagy Autophagy - drug effects Blotting, Western Cancer Cancer therapies Cell Line, Tumor Chemotherapy Cytotoxicity drug effects genes green fluorescent protein Hematology, Oncology and Palliative Medicine Humans Lung cancer organelles Paclitaxel Paclitaxel - pharmacology pharmacology Proteins RNA Interference RNA, Small Interfering small interfering RNA Lung cancer AVOs Paclitaxel 3-MA MTT LC3 Autophagy Apoptosis microtubule-associated protein 1 light chain 3 acidic vesicular organelles 3-methyladenine 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazoliumbromide
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Abstract	Paclitaxel has been demonstrated to be an effective mitotic inhibitor and apoptosis inducer to treat aggressive malignancies. In this paper, we have provided a line of evidence that promotion of apoptotic cell death by paclitaxel was accompanied with induction of autophagy in A549 cells. Paclitaxel treatment could lead to the formation of acidic vesicular organelles (AVOs), the induction of Atg5, Beclin 1 and microtubule-associated protein 1 light chain 3 (LC3) expressions, and the increase of punctate fluorescent signals in A549 cells pre-transfected with green fluorescent protein (GFP)-tagged LC3. Interestingly, paclitaxel-mediated apoptotic cell death was further potentiated by pretreatment with autophagy inhibitor 3-methyladenine (3-MA) or small interfering RNA against the autophagic gene beclin 1. These findings suggest that paclitaxel-elicited autophagic response plays a protective role that impedes the eventual cell death, and inhibition of autophagy could be an adjunctive strategy for enhancing chemotherapeutic effect of paclitaxel as an antitumor agent.
AbstractList	Paclitaxel has been demonstrated to be an effective mitotic inhibitor and apoptosis inducer to treat aggressive malignancies. In this paper, we have provided a line of evidence that promotion of apoptotic cell death by paclitaxel was accompanied with induction of autophagy in A549 cells. Paclitaxel treatment could lead to the formation of acidic vesicular organelles (AVOs), the induction of Atg5, Beclin 1 and microtubule-associated protein 1 light chain 3 (LC3) expressions, and the increase of punctate fluorescent signals in A549 cells pre-transfected with green fluorescent protein (GFP)-tagged LC3. Interestingly, paclitaxel-mediated apoptotic cell death was further potentiated by pretreatment with autophagy inhibitor 3-methyladenine (3-MA) or small interfering RNA against the autophagic gene beclin 1. These findings suggest that paclitaxel-elicited autophagic response plays a protective role that impedes the eventual cell death, and inhibition of autophagy could be an adjunctive strategy for enhancing chemotherapeutic effect of paclitaxel as an antitumor agent. Paclitaxel has been demonstrated to be an effective mitotic inhibitor and apoptosis inducer to treat aggressive malignancies. In this paper, we have provided a line of evidence that promotion of apoptotic cell death by paclitaxel was accompanied with induction of autophagy in A549 cells. Paclitaxel treatment could lead to the formation of acidic vesicular organelles (AVOs), the induction of Atg5, Beclin 1 and microtubule-associated protein 1 light chain 3 (LC3) expressions, and the increase of punctate fluorescent signals in A549 cells pre-transfected with green fluorescent protein (GFP)-tagged LC3. Interestingly, paclitaxel-mediated apoptotic cell death was further potentiated by pretreatment with autophagy inhibitor 3-methyladenine (3-MA) or small interfering RNA against the autophagic gene beclin1. These findings suggest that paclitaxel-elicited autophagic response plays a protective role that impedes the eventual cell death, and inhibition of autophagy could be an adjunctive strategy for enhancing chemotherapeutic effect of paclitaxel as an antitumor agent. Paclitaxel has been demonstrated to be an effective mitotic inhibitor and apoptosis inducer to treat aggressive malignancies. In this paper, we have provided a line of evidence that promotion of apoptotic cell death by paclitaxel was accompanied with induction of autophagy in A549 cells. Paclitaxel treatment could lead to the formation of acidic vesicular organelles (AVOs), the induction of Atg5, Beclin 1 and microtubule-associated protein 1 light chain 3 (LC3) expressions, and the increase of punctate fluorescent signals in A549 cells pre-transfected with green fluorescent protein (GFP)-tagged LC3. Interestingly, paclitaxel-mediated apoptotic cell death was further potentiated by pretreatment with autophagy inhibitor 3-methyladenine (3-MA) or small interfering RNA against the autophagic genebeclin1. These findings suggest that paclitaxel-elicited autophagic response plays a protective role that impedes the eventual cell death, and inhibition of autophagy could be an adjunctive strategy for enhancing chemotherapeutic effect of paclitaxel as an antitumor agent. Abstract Paclitaxel has been demonstrated to be an effective mitotic inhibitor and apoptosis inducer to treat aggressive malignancies. In this paper, we have provided a line of evidence that promotion of apoptotic cell death by paclitaxel was accompanied with induction of autophagy in A549 cells. Paclitaxel treatment could lead to the formation of acidic vesicular organelles (AVOs), the induction of Atg5, Beclin 1 and microtubule-associated protein 1 light chain 3 (LC3) expressions, and the increase of punctate fluorescent signals in A549 cells pre-transfected with green fluorescent protein (GFP)-tagged LC3. Interestingly, paclitaxel-mediated apoptotic cell death was further potentiated by pretreatment with autophagy inhibitor 3-methyladenine (3-MA) or small interfering RNA against the autophagic gene beclin 1 . These findings suggest that paclitaxel-elicited autophagic response plays a protective role that impedes the eventual cell death, and inhibition of autophagy could be an adjunctive strategy for enhancing chemotherapeutic effect of paclitaxel as an antitumor agent. Paclitaxel has been demonstrated to be an effective mitotic inhibitor and apoptosis inducer to treat aggressive malignancies. In this paper, we have provided a line of evidence that promotion of apoptotic cell death by paclitaxel was accompanied with induction of autophagy in A549 cells. Paclitaxel treatment could lead to the formation of acidic vesicular organelles (AVOs), the induction of Atg5, Beclin 1 and microtubule-associated protein 1 light chain 3 (LC3) expressions, and the increase of punctate fluorescent signals in A549 cells pre-transfected with green fluorescent protein (GFP)-tagged LC3. Interestingly, paclitaxel-mediated apoptotic cell death was further potentiated by pretreatment with autophagy inhibitor 3-methyladenine (3-MA) or small interfering RNA against the autophagic gene beclin1. These findings suggest that paclitaxel-elicited autophagic response plays a protective role that impedes the eventual cell death, and inhibition of autophagy could be an adjunctive strategy for enhancing chemotherapeutic effect of paclitaxel as an antitumor agent.Paclitaxel has been demonstrated to be an effective mitotic inhibitor and apoptosis inducer to treat aggressive malignancies. In this paper, we have provided a line of evidence that promotion of apoptotic cell death by paclitaxel was accompanied with induction of autophagy in A549 cells. Paclitaxel treatment could lead to the formation of acidic vesicular organelles (AVOs), the induction of Atg5, Beclin 1 and microtubule-associated protein 1 light chain 3 (LC3) expressions, and the increase of punctate fluorescent signals in A549 cells pre-transfected with green fluorescent protein (GFP)-tagged LC3. Interestingly, paclitaxel-mediated apoptotic cell death was further potentiated by pretreatment with autophagy inhibitor 3-methyladenine (3-MA) or small interfering RNA against the autophagic gene beclin1. These findings suggest that paclitaxel-elicited autophagic response plays a protective role that impedes the eventual cell death, and inhibition of autophagy could be an adjunctive strategy for enhancing chemotherapeutic effect of paclitaxel as an antitumor agent.
Author	Jiang, Hanming Young, Charles Y.F. Wu, Baolin Yuan, Huiqing Xi, Guangmin Pang, Yingxin Hu, Xiaoyan
Author_xml	– sequence: 1 givenname: Guangmin surname: Xi fullname: Xi, Guangmin organization: Department of Biochemistry and Molecular Biology, Shandong University School of Medicine, Jinan 250012, China – sequence: 2 givenname: Xiaoyan surname: Hu fullname: Hu, Xiaoyan organization: Department of Biochemistry and Molecular Biology, Shandong University School of Medicine, Jinan 250012, China – sequence: 3 givenname: Baolin surname: Wu fullname: Wu, Baolin organization: Department of Biochemistry and Chemistry, The Ohio State University, Columbus, OH 43210, USA – sequence: 4 givenname: Hanming surname: Jiang fullname: Jiang, Hanming organization: Department of Biochemistry and Molecular Biology, Shandong University School of Medicine, Jinan 250012, China – sequence: 5 givenname: Charles Y.F. surname: Young fullname: Young, Charles Y.F. organization: Department of Urology, Mayo Clinical College of Medicine, Mayo Clinic, Rochester, MN 55905, USA – sequence: 6 givenname: Yingxin surname: Pang fullname: Pang, Yingxin organization: Department of Biochemistry and Molecular Biology, Shandong University School of Medicine, Jinan 250012, China – sequence: 7 givenname: Huiqing surname: Yuan fullname: Yuan, Huiqing email: lyuanhq@sdu.edu.cn organization: Department of Biochemistry and Molecular Biology, Shandong University School of Medicine, Jinan 250012, China
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/21511395$$D View this record in MEDLINE/PubMed
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Keywords	Lung cancer AVOs Paclitaxel 3-MA MTT LC3 Autophagy Apoptosis microtubule-associated protein 1 light chain 3 acidic vesicular organelles 3-methyladenine 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazoliumbromide
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Snippet	Paclitaxel has been demonstrated to be an effective mitotic inhibitor and apoptosis inducer to treat aggressive malignancies. In this paper, we have provided a... Abstract Paclitaxel has been demonstrated to be an effective mitotic inhibitor and apoptosis inducer to treat aggressive malignancies. In this paper, we have...
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SubjectTerms	Antibiotics Antineoplastic Agents, Phytogenic Antineoplastic Agents, Phytogenic - pharmacology Apoptosis Apoptosis - drug effects Autophagy Autophagy - drug effects Blotting, Western Cancer Cancer therapies Cell Line, Tumor Chemotherapy Cytotoxicity drug effects genes green fluorescent protein Hematology, Oncology and Palliative Medicine Humans Lung cancer organelles Paclitaxel Paclitaxel - pharmacology pharmacology Proteins RNA Interference RNA, Small Interfering small interfering RNA
Title	Autophagy inhibition promotes paclitaxel-induced apoptosis in cancer cells
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