Mitophagy promotes sorafenib resistance through hypoxia-inducible ATAD3A dependent Axis

Background The identification of novel targets for recovering sorafenib resistance is pivotal for Hepatocellular carcinoma (HCC) patients. Mitophagy is the programmed degradation of mitochondria, and is likely involved in drug resistance of cancer cells. Here, we identified hyperactivated mitophagy...

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Published inJournal of experimental & clinical cancer research Vol. 39; no. 1; pp. 274 - 16
Main Authors Wu, Hong, Wang, Tao, Liu, Yiqiang, Li, Xin, Xu, Senlin, Wu, Changtao, Zou, Hongbo, Cao, Mianfu, Jin, Guoxiang, Lang, Jinyi, Wang, Bin, Liu, Baohua, Luo, Xiaolin, Xu, Chuan
Format Journal Article
LanguageEnglish
Published London BioMed Central 07.12.2020
BioMed Central Ltd
BMC
Subjects
Adenosine triphosphatase
Angiogenesis
Animals
Antibodies
Antineoplastic Agents - pharmacology
Apoptosis
ATAD3A
ATPases Associated with Diverse Cellular Activities - metabolism
Autophagy
Biomedical and Life Sciences
Biomedicine
Cancer Research
Cancer therapies
Cell Line, Tumor
Drug resistance
Drug Resistance, Neoplasm
Female
Gene expression
Genes
Growth factors
Humans
Hypoxia
Hypoxia and Tumors
Immunology
Inhibitor drugs
Kinases
Liver cancer
Liver Neoplasms - drug therapy
Liver Neoplasms - metabolism
Liver Neoplasms - pathology
Membrane Proteins - metabolism
Mice
Mice, Inbred BALB C
Mice, Nude
Mitochondrial Proteins - metabolism
Mitophagy
Mitophagy - drug effects
Oncology
Proteins
RNA
RNA sequencing
Sorafenib - pharmacology
Sorafenib resistance
Targeted cancer therapy
Tumor Hypoxia - physiology
Tumors
Beijing China
United States > US
China
Hypoxia
Sorafenib resistance
Mitophagy
ATAD3A
Online AccessGet full text
ISSN1756-9966
0392-9078
1756-9966
DOI10.1186/s13046-020-01768-8

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Abstract Background The identification of novel targets for recovering sorafenib resistance is pivotal for Hepatocellular carcinoma (HCC) patients. Mitophagy is the programmed degradation of mitochondria, and is likely involved in drug resistance of cancer cells. Here, we identified hyperactivated mitophagy is essential for sorafenib resistance, and the mitophagy core regulator gene ATAD3A (ATPase family AAA domain containing 3A) was down regulated in hypoxia induced resistant HCC cells. Blocking mitophagy may restore the sorafenib sensitivity of these cells and provide a new treatment strategy for HCC patients. Methods Hypoxia induced sorafenib resistant cancer cells were established by culturing under 1% O 2 with increasing drug treatment. RNA sequencing was conducted in transfecting LM3 cells with sh-ATAD3A lentivirus. Subsequent mechanistic studies were performed in HCC cell lines by manipulating ATAD3A expression isogenically where we evaluated drug sensitivity, molecular signaling events. In vivo study, we investigated the combined treatment effect of sorafenib and miR-210-5P antagomir. Results We found a hyperactivated mitophagy regulating by ATAD3A-PINK1/PARKIN axis in hypoxia induced sorafenib resistant HCC cells. Gain- and loss- of ATAD3A were related to hypoxia-induced mitophagy and sorafenib resistance. In addition, ATAD3A is a functional target of miR-210-5p and its oncogenic functions are likely mediated by increased miR-210-5P expression. miR-210-5P was upregulated under hypoxia and participated in regulating sorafenib resistance. In vivo xenograft assay showed that miR-210-5P antagomir combined with sorafenib abrogated the tumorigenic effect of ATAD3A down-regulation in mice. Conclusions Loss of ATAD3A hyperactivates mitophagy which is a core event in hypoxia induced sorafenib resistance in HCC cells. Targeting miR-210-5P-ATAD3A axis is a novel therapeutic target for sorafenib-resistant HCC.
AbstractList The identification of novel targets for recovering sorafenib resistance is pivotal for Hepatocellular carcinoma (HCC) patients. Mitophagy is the programmed degradation of mitochondria, and is likely involved in drug resistance of cancer cells. Here, we identified hyperactivated mitophagy is essential for sorafenib resistance, and the mitophagy core regulator gene ATAD3A (ATPase family AAA domain containing 3A) was down regulated in hypoxia induced resistant HCC cells. Blocking mitophagy may restore the sorafenib sensitivity of these cells and provide a new treatment strategy for HCC patients. Hypoxia induced sorafenib resistant cancer cells were established by culturing under 1% O.sub.2 with increasing drug treatment. RNA sequencing was conducted in transfecting LM3 cells with sh-ATAD3A lentivirus. Subsequent mechanistic studies were performed in HCC cell lines by manipulating ATAD3A expression isogenically where we evaluated drug sensitivity, molecular signaling events. In vivo study, we investigated the combined treatment effect of sorafenib and miR-210-5P antagomir. We found a hyperactivated mitophagy regulating by ATAD3A-PINK1/PARKIN axis in hypoxia induced sorafenib resistant HCC cells. Gain- and loss- of ATAD3A were related to hypoxia-induced mitophagy and sorafenib resistance. In addition, ATAD3A is a functional target of miR-210-5p and its oncogenic functions are likely mediated by increased miR-210-5P expression. miR-210-5P was upregulated under hypoxia and participated in regulating sorafenib resistance. In vivo xenograft assay showed that miR-210-5P antagomir combined with sorafenib abrogated the tumorigenic effect of ATAD3A down-regulation in mice. Loss of ATAD3A hyperactivates mitophagy which is a core event in hypoxia induced sorafenib resistance in HCC cells. Targeting miR-210-5P-ATAD3A axis is a novel therapeutic target for sorafenib-resistant HCC.
Background The identification of novel targets for recovering sorafenib resistance is pivotal for Hepatocellular carcinoma (HCC) patients. Mitophagy is the programmed degradation of mitochondria, and is likely involved in drug resistance of cancer cells. Here, we identified hyperactivated mitophagy is essential for sorafenib resistance, and the mitophagy core regulator gene ATAD3A (ATPase family AAA domain containing 3A) was down regulated in hypoxia induced resistant HCC cells. Blocking mitophagy may restore the sorafenib sensitivity of these cells and provide a new treatment strategy for HCC patients. Methods Hypoxia induced sorafenib resistant cancer cells were established by culturing under 1% O 2 with increasing drug treatment. RNA sequencing was conducted in transfecting LM3 cells with sh-ATAD3A lentivirus. Subsequent mechanistic studies were performed in HCC cell lines by manipulating ATAD3A expression isogenically where we evaluated drug sensitivity, molecular signaling events. In vivo study, we investigated the combined treatment effect of sorafenib and miR-210-5P antagomir. Results We found a hyperactivated mitophagy regulating by ATAD3A-PINK1/PARKIN axis in hypoxia induced sorafenib resistant HCC cells. Gain- and loss- of ATAD3A were related to hypoxia-induced mitophagy and sorafenib resistance. In addition, ATAD3A is a functional target of miR-210-5p and its oncogenic functions are likely mediated by increased miR-210-5P expression. miR-210-5P was upregulated under hypoxia and participated in regulating sorafenib resistance. In vivo xenograft assay showed that miR-210-5P antagomir combined with sorafenib abrogated the tumorigenic effect of ATAD3A down-regulation in mice. Conclusions Loss of ATAD3A hyperactivates mitophagy which is a core event in hypoxia induced sorafenib resistance in HCC cells. Targeting miR-210-5P-ATAD3A axis is a novel therapeutic target for sorafenib-resistant HCC.
Background The identification of novel targets for recovering sorafenib resistance is pivotal for Hepatocellular carcinoma (HCC) patients. Mitophagy is the programmed degradation of mitochondria, and is likely involved in drug resistance of cancer cells. Here, we identified hyperactivated mitophagy is essential for sorafenib resistance, and the mitophagy core regulator gene ATAD3A (ATPase family AAA domain containing 3A) was down regulated in hypoxia induced resistant HCC cells. Blocking mitophagy may restore the sorafenib sensitivity of these cells and provide a new treatment strategy for HCC patients. Methods Hypoxia induced sorafenib resistant cancer cells were established by culturing under 1% O2 with increasing drug treatment. RNA sequencing was conducted in transfecting LM3 cells with sh-ATAD3A lentivirus. Subsequent mechanistic studies were performed in HCC cell lines by manipulating ATAD3A expression isogenically where we evaluated drug sensitivity, molecular signaling events. In vivo study, we investigated the combined treatment effect of sorafenib and miR-210-5P antagomir. Results We found a hyperactivated mitophagy regulating by ATAD3A-PINK1/PARKIN axis in hypoxia induced sorafenib resistant HCC cells. Gain- and loss- of ATAD3A were related to hypoxia-induced mitophagy and sorafenib resistance. In addition, ATAD3A is a functional target of miR-210-5p and its oncogenic functions are likely mediated by increased miR-210-5P expression. miR-210-5P was upregulated under hypoxia and participated in regulating sorafenib resistance. In vivo xenograft assay showed that miR-210-5P antagomir combined with sorafenib abrogated the tumorigenic effect of ATAD3A down-regulation in mice. Conclusions Loss of ATAD3A hyperactivates mitophagy which is a core event in hypoxia induced sorafenib resistance in HCC cells. Targeting miR-210-5P-ATAD3A axis is a novel therapeutic target for sorafenib-resistant HCC.
Abstract Background The identification of novel targets for recovering sorafenib resistance is pivotal for Hepatocellular carcinoma (HCC) patients. Mitophagy is the programmed degradation of mitochondria, and is likely involved in drug resistance of cancer cells. Here, we identified hyperactivated mitophagy is essential for sorafenib resistance, and the mitophagy core regulator gene ATAD3A (ATPase family AAA domain containing 3A) was down regulated in hypoxia induced resistant HCC cells. Blocking mitophagy may restore the sorafenib sensitivity of these cells and provide a new treatment strategy for HCC patients. Methods Hypoxia induced sorafenib resistant cancer cells were established by culturing under 1% O2 with increasing drug treatment. RNA sequencing was conducted in transfecting LM3 cells with sh-ATAD3A lentivirus. Subsequent mechanistic studies were performed in HCC cell lines by manipulating ATAD3A expression isogenically where we evaluated drug sensitivity, molecular signaling events. In vivo study, we investigated the combined treatment effect of sorafenib and miR-210-5P antagomir. Results We found a hyperactivated mitophagy regulating by ATAD3A-PINK1/PARKIN axis in hypoxia induced sorafenib resistant HCC cells. Gain- and loss- of ATAD3A were related to hypoxia-induced mitophagy and sorafenib resistance. In addition, ATAD3A is a functional target of miR-210-5p and its oncogenic functions are likely mediated by increased miR-210-5P expression. miR-210-5P was upregulated under hypoxia and participated in regulating sorafenib resistance. In vivo xenograft assay showed that miR-210-5P antagomir combined with sorafenib abrogated the tumorigenic effect of ATAD3A down-regulation in mice. Conclusions Loss of ATAD3A hyperactivates mitophagy which is a core event in hypoxia induced sorafenib resistance in HCC cells. Targeting miR-210-5P-ATAD3A axis is a novel therapeutic target for sorafenib-resistant HCC.
Background The identification of novel targets for recovering sorafenib resistance is pivotal for Hepatocellular carcinoma (HCC) patients. Mitophagy is the programmed degradation of mitochondria, and is likely involved in drug resistance of cancer cells. Here, we identified hyperactivated mitophagy is essential for sorafenib resistance, and the mitophagy core regulator gene ATAD3A (ATPase family AAA domain containing 3A) was down regulated in hypoxia induced resistant HCC cells. Blocking mitophagy may restore the sorafenib sensitivity of these cells and provide a new treatment strategy for HCC patients. Methods Hypoxia induced sorafenib resistant cancer cells were established by culturing under 1% O.sub.2 with increasing drug treatment. RNA sequencing was conducted in transfecting LM3 cells with sh-ATAD3A lentivirus. Subsequent mechanistic studies were performed in HCC cell lines by manipulating ATAD3A expression isogenically where we evaluated drug sensitivity, molecular signaling events. In vivo study, we investigated the combined treatment effect of sorafenib and miR-210-5P antagomir. Results We found a hyperactivated mitophagy regulating by ATAD3A-PINK1/PARKIN axis in hypoxia induced sorafenib resistant HCC cells. Gain- and loss- of ATAD3A were related to hypoxia-induced mitophagy and sorafenib resistance. In addition, ATAD3A is a functional target of miR-210-5p and its oncogenic functions are likely mediated by increased miR-210-5P expression. miR-210-5P was upregulated under hypoxia and participated in regulating sorafenib resistance. In vivo xenograft assay showed that miR-210-5P antagomir combined with sorafenib abrogated the tumorigenic effect of ATAD3A down-regulation in mice. Conclusions Loss of ATAD3A hyperactivates mitophagy which is a core event in hypoxia induced sorafenib resistance in HCC cells. Targeting miR-210-5P-ATAD3A axis is a novel therapeutic target for sorafenib-resistant HCC. Keywords: Mitophagy, ATAD3A, Hypoxia, Sorafenib resistance
The identification of novel targets for recovering sorafenib resistance is pivotal for Hepatocellular carcinoma (HCC) patients. Mitophagy is the programmed degradation of mitochondria, and is likely involved in drug resistance of cancer cells. Here, we identified hyperactivated mitophagy is essential for sorafenib resistance, and the mitophagy core regulator gene ATAD3A (ATPase family AAA domain containing 3A) was down regulated in hypoxia induced resistant HCC cells. Blocking mitophagy may restore the sorafenib sensitivity of these cells and provide a new treatment strategy for HCC patients. Hypoxia induced sorafenib resistant cancer cells were established by culturing under 1% O with increasing drug treatment. RNA sequencing was conducted in transfecting LM3 cells with sh-ATAD3A lentivirus. Subsequent mechanistic studies were performed in HCC cell lines by manipulating ATAD3A expression isogenically where we evaluated drug sensitivity, molecular signaling events. In vivo study, we investigated the combined treatment effect of sorafenib and miR-210-5P antagomir. We found a hyperactivated mitophagy regulating by ATAD3A-PINK1/PARKIN axis in hypoxia induced sorafenib resistant HCC cells. Gain- and loss- of ATAD3A were related to hypoxia-induced mitophagy and sorafenib resistance. In addition, ATAD3A is a functional target of miR-210-5p and its oncogenic functions are likely mediated by increased miR-210-5P expression. miR-210-5P was upregulated under hypoxia and participated in regulating sorafenib resistance. In vivo xenograft assay showed that miR-210-5P antagomir combined with sorafenib abrogated the tumorigenic effect of ATAD3A down-regulation in mice. Loss of ATAD3A hyperactivates mitophagy which is a core event in hypoxia induced sorafenib resistance in HCC cells. Targeting miR-210-5P-ATAD3A axis is a novel therapeutic target for sorafenib-resistant HCC.
The identification of novel targets for recovering sorafenib resistance is pivotal for Hepatocellular carcinoma (HCC) patients. Mitophagy is the programmed degradation of mitochondria, and is likely involved in drug resistance of cancer cells. Here, we identified hyperactivated mitophagy is essential for sorafenib resistance, and the mitophagy core regulator gene ATAD3A (ATPase family AAA domain containing 3A) was down regulated in hypoxia induced resistant HCC cells. Blocking mitophagy may restore the sorafenib sensitivity of these cells and provide a new treatment strategy for HCC patients.BACKGROUNDThe identification of novel targets for recovering sorafenib resistance is pivotal for Hepatocellular carcinoma (HCC) patients. Mitophagy is the programmed degradation of mitochondria, and is likely involved in drug resistance of cancer cells. Here, we identified hyperactivated mitophagy is essential for sorafenib resistance, and the mitophagy core regulator gene ATAD3A (ATPase family AAA domain containing 3A) was down regulated in hypoxia induced resistant HCC cells. Blocking mitophagy may restore the sorafenib sensitivity of these cells and provide a new treatment strategy for HCC patients.Hypoxia induced sorafenib resistant cancer cells were established by culturing under 1% O2 with increasing drug treatment. RNA sequencing was conducted in transfecting LM3 cells with sh-ATAD3A lentivirus. Subsequent mechanistic studies were performed in HCC cell lines by manipulating ATAD3A expression isogenically where we evaluated drug sensitivity, molecular signaling events. In vivo study, we investigated the combined treatment effect of sorafenib and miR-210-5P antagomir.METHODSHypoxia induced sorafenib resistant cancer cells were established by culturing under 1% O2 with increasing drug treatment. RNA sequencing was conducted in transfecting LM3 cells with sh-ATAD3A lentivirus. Subsequent mechanistic studies were performed in HCC cell lines by manipulating ATAD3A expression isogenically where we evaluated drug sensitivity, molecular signaling events. In vivo study, we investigated the combined treatment effect of sorafenib and miR-210-5P antagomir.We found a hyperactivated mitophagy regulating by ATAD3A-PINK1/PARKIN axis in hypoxia induced sorafenib resistant HCC cells. Gain- and loss- of ATAD3A were related to hypoxia-induced mitophagy and sorafenib resistance. In addition, ATAD3A is a functional target of miR-210-5p and its oncogenic functions are likely mediated by increased miR-210-5P expression. miR-210-5P was upregulated under hypoxia and participated in regulating sorafenib resistance. In vivo xenograft assay showed that miR-210-5P antagomir combined with sorafenib abrogated the tumorigenic effect of ATAD3A down-regulation in mice.RESULTSWe found a hyperactivated mitophagy regulating by ATAD3A-PINK1/PARKIN axis in hypoxia induced sorafenib resistant HCC cells. Gain- and loss- of ATAD3A were related to hypoxia-induced mitophagy and sorafenib resistance. In addition, ATAD3A is a functional target of miR-210-5p and its oncogenic functions are likely mediated by increased miR-210-5P expression. miR-210-5P was upregulated under hypoxia and participated in regulating sorafenib resistance. In vivo xenograft assay showed that miR-210-5P antagomir combined with sorafenib abrogated the tumorigenic effect of ATAD3A down-regulation in mice.Loss of ATAD3A hyperactivates mitophagy which is a core event in hypoxia induced sorafenib resistance in HCC cells. Targeting miR-210-5P-ATAD3A axis is a novel therapeutic target for sorafenib-resistant HCC.CONCLUSIONSLoss of ATAD3A hyperactivates mitophagy which is a core event in hypoxia induced sorafenib resistance in HCC cells. Targeting miR-210-5P-ATAD3A axis is a novel therapeutic target for sorafenib-resistant HCC.
ArticleNumber 274
Audience Academic
Author Liu, Baohua
Liu, Yiqiang
Xu, Senlin
Luo, Xiaolin
Wu, Hong
Wang, Tao
Zou, Hongbo
Cao, Mianfu
Li, Xin
Wang, Bin
Wu, Changtao
Xu, Chuan
Lang, Jinyi
Jin, Guoxiang
Author_xml – sequence: 1
  givenname: Hong
  surname: Wu
  fullname: Wu, Hong
  organization: Guangdong Key Laboratory of Genome Stability and Human Disease Prevention, Shenzhen University Health Science Center, Integrative Cancer Center&Cancer Clinical Research Center, Sichuan Cancer Hospital & Institute Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Department of Experimental Research, The Affiliated Tumor Hospital of Guangxi Medical University
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  givenname: Tao
  surname: Wang
  fullname: Wang, Tao
  organization: Department of Gastroenterology, Daping Hospital, Army Medical University (Third Military Medical University)
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  givenname: Yiqiang
  surname: Liu
  fullname: Liu, Yiqiang
  organization: Integrative Cancer Center&Cancer Clinical Research Center, Sichuan Cancer Hospital & Institute Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Department of Experimental Research, The Affiliated Tumor Hospital of Guangxi Medical University
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  givenname: Xin
  surname: Li
  fullname: Li, Xin
  organization: Department of Experimental Research, The Affiliated Tumor Hospital of Guangxi Medical University
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  givenname: Senlin
  surname: Xu
  fullname: Xu, Senlin
  organization: Institute of Pathology and Southwest Cancer Center, Southwest Hospital and Key Laboratory of Tumor Immunopathology, Army Medical University (Third Military Medical University)
– sequence: 6
  givenname: Changtao
  surname: Wu
  fullname: Wu, Changtao
  organization: Integrative Cancer Center&Cancer Clinical Research Center, Sichuan Cancer Hospital & Institute Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Department of Experimental Research, The Affiliated Tumor Hospital of Guangxi Medical University
– sequence: 7
  givenname: Hongbo
  surname: Zou
  fullname: Zou, Hongbo
  organization: Institute of Pathology and Southwest Cancer Center, Southwest Hospital and Key Laboratory of Tumor Immunopathology, Army Medical University (Third Military Medical University)
– sequence: 8
  givenname: Mianfu
  surname: Cao
  fullname: Cao, Mianfu
  organization: Institute of Pathology and Southwest Cancer Center, Southwest Hospital and Key Laboratory of Tumor Immunopathology, Army Medical University (Third Military Medical University)
– sequence: 9
  givenname: Guoxiang
  surname: Jin
  fullname: Jin, Guoxiang
  organization: Institute of Pathology and Southwest Cancer Center, Southwest Hospital and Key Laboratory of Tumor Immunopathology, Army Medical University (Third Military Medical University)
– sequence: 10
  givenname: Jinyi
  surname: Lang
  fullname: Lang, Jinyi
  organization: Integrative Cancer Center&Cancer Clinical Research Center, Sichuan Cancer Hospital & Institute Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China
– sequence: 11
  givenname: Bin
  surname: Wang
  fullname: Wang, Bin
  organization: Department of Gastroenterology, Daping Hospital, Army Medical University (Third Military Medical University)
– sequence: 12
  givenname: Baohua
  surname: Liu
  fullname: Liu, Baohua
  email: ppliew@szu.edu.cn
  organization: Guangdong Key Laboratory of Genome Stability and Human Disease Prevention, Shenzhen University Health Science Center
– sequence: 13
  givenname: Xiaolin
  surname: Luo
  fullname: Luo, Xiaolin
  email: luoxiaoling67@126.com
  organization: Department of Experimental Research, The Affiliated Tumor Hospital of Guangxi Medical University
– sequence: 14
  givenname: Chuan
  surname: Xu
  fullname: Xu, Chuan
  email: xuchuan100@uestc.edu.cn
  organization: Integrative Cancer Center&Cancer Clinical Research Center, Sichuan Cancer Hospital & Institute Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China
BackLink https://www.ncbi.nlm.nih.gov/pubmed/33280610$$D View this record in MEDLINE/PubMed
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Issue 1
Keywords Hypoxia
Sorafenib resistance
Mitophagy
ATAD3A
Language English
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Snippet Background The identification of novel targets for recovering sorafenib resistance is pivotal for Hepatocellular carcinoma (HCC) patients. Mitophagy is the...
The identification of novel targets for recovering sorafenib resistance is pivotal for Hepatocellular carcinoma (HCC) patients. Mitophagy is the programmed...
Background The identification of novel targets for recovering sorafenib resistance is pivotal for Hepatocellular carcinoma (HCC) patients. Mitophagy is the...
Abstract Background The identification of novel targets for recovering sorafenib resistance is pivotal for Hepatocellular carcinoma (HCC) patients. Mitophagy...
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StartPage 274
SubjectTerms Adenosine triphosphatase
Angiogenesis
Animals
Antibodies
Antineoplastic Agents - pharmacology
Apoptosis
ATAD3A
ATPases Associated with Diverse Cellular Activities - metabolism
Autophagy
Biomedical and Life Sciences
Biomedicine
Cancer Research
Cancer therapies
Cell Line, Tumor
Drug resistance
Drug Resistance, Neoplasm
Female
Gene expression
Genes
Growth factors
Humans
Hypoxia
Hypoxia and Tumors
Immunology
Inhibitor drugs
Kinases
Liver cancer
Liver Neoplasms - drug therapy
Liver Neoplasms - metabolism
Liver Neoplasms - pathology
Membrane Proteins - metabolism
Mice
Mice, Inbred BALB C
Mice, Nude
Mitochondrial Proteins - metabolism
Mitophagy
Mitophagy - drug effects
Oncology
Proteins
RNA
RNA sequencing
Sorafenib - pharmacology
Sorafenib resistance
Targeted cancer therapy
Tumor Hypoxia - physiology
Tumors
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Title Mitophagy promotes sorafenib resistance through hypoxia-inducible ATAD3A dependent Axis
URI https://link.springer.com/article/10.1186/s13046-020-01768-8
https://www.ncbi.nlm.nih.gov/pubmed/33280610
https://www.proquest.com/docview/2471138388
https://www.proquest.com/docview/2467846942
https://pubmed.ncbi.nlm.nih.gov/PMC7720487
https://doaj.org/article/7502d60c10d24f09a3b4be155bd4be68
Volume 39
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