ChloroquineV1, Main, Exploration, bibRecord, 000D51

The induction of autophagy against mitochondria-mediated apoptosis in lung cancer cells by a ruthenium (II) imidazole complex.

Identifieur interne : 000D51 ( Main/Exploration ); précédent : 000D50; suivant : 000D52

The induction of autophagy against mitochondria-mediated apoptosis in lung cancer cells by a ruthenium (II) imidazole complex.

Source :

Oncotarget [ 1949-2553 ] ; 2016.

RBID : pubmed:27811372

Descripteurs français

English descriptors

KwdEn :
- A549 Cells, Animals, Antineoplastic Agents (pharmacology), Apoptosis (drug effects), Autophagosomes (drug effects), Autophagosomes (metabolism), Autophagosomes (pathology), Autophagy (drug effects), Caspase 3 (metabolism), Cell Cycle Checkpoints (drug effects), Cell Proliferation (drug effects), Cytochromes c (metabolism), Dose-Response Relationship, Drug, Extracellular Signal-Regulated MAP Kinases (metabolism), Female, Humans, Imidazoles (pharmacology), Lung Neoplasms (drug therapy), Lung Neoplasms (metabolism), Lung Neoplasms (pathology), Mice, Inbred BALB C, Mice, Nude, Microtubule-Associated Proteins (metabolism), Mitochondria (drug effects), Mitochondria (metabolism), Mitochondria (pathology), Organometallic Compounds (pharmacology), Reactive Oxygen Species (metabolism), Ruthenium (pharmacology), Signal Transduction (drug effects), Time Factors, Tumor Burden (drug effects), Xenograft Model Antitumor Assays.
MESH :
- chemical , metabolism : Caspase 3, Cytochromes c, Extracellular Signal-Regulated MAP Kinases, Microtubule-Associated Proteins, Reactive Oxygen Species.
- chemical , pharmacology : Antineoplastic Agents, Imidazoles, Organometallic Compounds, Ruthenium.
- drug effects : Apoptosis, Autophagosomes, Autophagy, Cell Cycle Checkpoints, Cell Proliferation, Mitochondria, Signal Transduction, Tumor Burden.
- drug therapy : Lung Neoplasms.
- metabolism : Autophagosomes, Lung Neoplasms, Mitochondria.
- pathology : Autophagosomes, Lung Neoplasms, Mitochondria.
- A549 Cells, Animals, Dose-Response Relationship, Drug, Female, Humans, Mice, Inbred BALB C, Mice, Nude, Time Factors, Xenograft Model Antitumor Assays.

Abstract

In the present study, it was found that the ruthenium (II) imidazole complex [Ru(Im)4(dppz)]2+ (Ru1) could induce significant growth inhibition and apoptosis in A549 and NCI-H460 cells. Apart from the induction of apoptosis, it was reported for the first time that Ru1 induced an autophagic response in A549 and NCI-H460 cells as evidenced by the formation of autophagosomes, acidic vesicular organelles (AVOs), and the up-regulation of LC3-II. Furthermore, scavenging of reactive oxygen species (ROS) by antioxidant NAC or Tiron inhibited the release of cytochrome c, caspase-3 activity, and eventually rescued cancer cells from Ru1-mediated apoptosis, suggesting that Ru1 inducing apoptosis was partially caspase 3-dependent by triggering ROS-mediated mitochondrial dysfunction in A549 and NCI-H460 cells. Further study indicated that the extracellular signal-regulated kinase (ERK) signaling pathway was involved in Ru1-induced autophagy in A549 and NCI-H460 cells. Moreover, blocking autophagy using pharmacological inhibitors 3-methyladenine (3-MA) and chloroquine (CQ) enhanced Ru1-induced apoptosis, indicating the cytoprotective role of autophagy in Ru1-treated A549 and NCI-H460 cells. Finally, the in vivo mice bearing A549 xenografts, Ru1 dosed at 10 or 20 mg/kg significantly inhibited tumor growth.

DOI: 10.18632/oncotarget.13032
PubMed: 27811372

Affiliations:

République populaire de Chine

Le document en format XML

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<front><div type="abstract" xml:lang="en">In the present study, it was found that the ruthenium (II) imidazole complex [Ru(Im)4(dppz)]2+ (Ru1) could induce significant growth inhibition and apoptosis in A549 and NCI-H460 cells. Apart from the induction of apoptosis, it was reported for the first time that Ru1 induced an autophagic response in A549 and NCI-H460 cells as evidenced by the formation of autophagosomes, acidic vesicular organelles (AVOs), and the up-regulation of LC3-II. Furthermore, scavenging of reactive oxygen species (ROS) by antioxidant NAC or Tiron inhibited the release of cytochrome c, caspase-3 activity, and eventually rescued cancer cells from Ru1-mediated apoptosis, suggesting that Ru1 inducing apoptosis was partially caspase 3-dependent by triggering ROS-mediated mitochondrial dysfunction in A549 and NCI-H460 cells. Further study indicated that the extracellular signal-regulated kinase (ERK) signaling pathway was involved in Ru1-induced autophagy in A549 and NCI-H460 cells. Moreover, blocking autophagy using pharmacological inhibitors 3-methyladenine (3-MA) and chloroquine (CQ) enhanced Ru1-induced apoptosis, indicating the cytoprotective role of autophagy in Ru1-treated A549 and NCI-H460 cells. Finally, the in vivo mice bearing A549 xenografts, Ru1 dosed at 10 or 20 mg/kg significantly inhibited tumor growth.</div>
</front>
</TEI>
<affiliations><list><country><li>République populaire de Chine</li>
</country>
</list>
<tree><country name="République populaire de Chine"><noRegion><name sortKey="Chen, Lanmei" sort="Chen, Lanmei" uniqKey="Chen L" first="Lanmei" last="Chen">Lanmei Chen</name>
</noRegion>
<name sortKey="Cai, Kangrong" sort="Cai, Kangrong" uniqKey="Cai K" first="Kangrong" last="Cai">Kangrong Cai</name>
<name sortKey="Chen, Jincan" sort="Chen, Jincan" uniqKey="Chen J" first="Jincan" last="Chen">Jincan Chen</name>
<name sortKey="Dongye, Guangzhi" sort="Dongye, Guangzhi" uniqKey="Dongye G" first="Guangzhi" last="Dongye">Guangzhi Dongye</name>
<name sortKey="Feng, Ruibing" sort="Feng, Ruibing" uniqKey="Feng R" first="Ruibing" last="Feng">Ruibing Feng</name>
<name sortKey="Jie, Xinming" sort="Jie, Xinming" uniqKey="Jie X" first="Xinming" last="Jie">Xinming Jie</name>
<name sortKey="Li, Baojun" sort="Li, Baojun" uniqKey="Li B" first="Baojun" last="Li">Baojun Li</name>
<name sortKey="Li, Guodong" sort="Li, Guodong" uniqKey="Li G" first="Guodong" last="Li">Guodong Li</name>
<name sortKey="Lun, Kaiyi" sort="Lun, Kaiyi" uniqKey="Lun K" first="Kaiyi" last="Lun">Kaiyi Lun</name>
<name sortKey="Peng, Fa" sort="Peng, Fa" uniqKey="Peng F" first="Fa" last="Peng">Fa Peng</name>
<name sortKey="Xu, Bilian" sort="Xu, Bilian" uniqKey="Xu B" first="Bilian" last="Xu">Bilian Xu</name>
<name sortKey="Zeng, Qingwang" sort="Zeng, Qingwang" uniqKey="Zeng Q" first="Qingwang" last="Zeng">Qingwang Zeng</name>
</country>
</tree>
</affiliations>
</record>

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The induction of autophagy against mitochondria-mediated apoptosis in lung cancer cells by a ruthenium (II) imidazole complex.

The induction of autophagy against mitochondria-mediated apoptosis in lung cancer cells by a ruthenium (II) imidazole complex.

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