PubTransformer

A site to transform Pubmed publications into these bibliographic reference formats: ADS, BibTeX, EndNote, ISI used by the Web of Knowledge, RIS, MEDLINE, Microsoft's Word 2007 XML.

Silencing of NRAGE induces autophagy via AMPK/Ulk1/Atg13 signaling pathway in NSCLC cells.

Abstract NRAGE has been reported to be overexpressed in cancer cells, especially in lung cancer cells. To determine the role of NRAGE in non-small-cell lung cancer cells, we investigated the effects of NRAGE on autophagy in non-small-cell lung cancer cells. Human A549 and H1299 cells were transfected with NRAGE-specific small-interfering RNA. The Cell Counting Kit-8 and plate clone assay showed that downregulation of NRAGE could induce the proliferation in A549 and H1299 cells. In addition, our data suggested that downregulation of NRAGE enhances autophagosome formation by immunofluorescence. We found that knockdown of NRAGE induced autophagy, together with downregulation of P62 and upregulation of LC3-II protein. Furthermore, to elucidate the mechanism of NRAGE in suppressing autophagy, the protein expressions of AMPK, Ulk1, and Atg13 were assessed. Collectively, these results demonstrate the effective anti-autophagic of NRAGE in non-small-cell lung cancer cells through AMPK/Ulk1/Atg13 autophagy signaling pathways. Therefore, NRAGE could be used as a potential therapeutic target for lung cancer.
PMID
Related Publications

The association of AMPK with ULK1 regulates autophagy.

ATG13: just a companion, or an executor of the autophagic program?

Silencing of EEF2K (eukaryotic elongation factor-2 kinase) reveals AMPK-ULK1-dependent autophagy in colon cancer cells.

ULK1.ATG13.FIP200 complex mediates mTOR signaling and is essential for autophagy.

ULK1 plays a critical role in AMPK-mediated myocardial autophagy and contractile dysfunction following acute alcohol challenge.

Authors

Mayor MeshTerms
Keywords

AMPK/Ulk1/Atg13 signaling pathway

NRAGE

autophagy

non-small-cell lung cancer

proliferation

Journal Title tumour biology : the journal of the international society for oncodevelopmental biology and medicine
Publication Year Start




PMID- 28639909
OWN - NLM
STAT- MEDLINE
DA  - 20170622
DCOM- 20170711
LR  - 20170713
IS  - 1423-0380 (Electronic)
IS  - 1010-4283 (Linking)
VI  - 39
IP  - 6
DP  - 2017 Jun
TI  - Silencing of NRAGE induces autophagy via AMPK/Ulk1/Atg13 signaling pathway in
      NSCLC cells.
PG  - 1010428317709676
LID - 10.1177/1010428317709676 [doi]
AB  - NRAGE has been reported to be overexpressed in cancer cells, especially in lung
      cancer cells. To determine the role of NRAGE in non-small-cell lung cancer cells,
      we investigated the effects of NRAGE on autophagy in non-small-cell lung cancer
      cells. Human A549 and H1299 cells were transfected with NRAGE-specific
      small-interfering RNA. The Cell Counting Kit-8 and plate clone assay showed that 
      downregulation of NRAGE could induce the proliferation in A549 and H1299 cells.
      In addition, our data suggested that downregulation of NRAGE enhances
      autophagosome formation by immunofluorescence. We found that knockdown of NRAGE
      induced autophagy, together with downregulation of P62 and upregulation of LC3-II
      protein. Furthermore, to elucidate the mechanism of NRAGE in suppressing
      autophagy, the protein expressions of AMPK, Ulk1, and Atg13 were assessed.
      Collectively, these results demonstrate the effective anti-autophagic of NRAGE in
      non-small-cell lung cancer cells through AMPK/Ulk1/Atg13 autophagy signaling
      pathways. Therefore, NRAGE could be used as a potential therapeutic target for
      lung cancer.
FAU - Zhou, Yiyang
AU  - Zhou Y
AD  - 1 Department of Oncology, Shanghai Municipal Hospital of Traditional Chinese
      Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
FAU - Huang, Nan
AU  - Huang N
AD  - 2 Department of Clinical Laboratory Medicine, Shanghai Tenth People's Hospital of
      Tongji University, Shanghai, China.
FAU - Wu, Jianchun
AU  - Wu J
AD  - 1 Department of Oncology, Shanghai Municipal Hospital of Traditional Chinese
      Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
FAU - Zhen, Ni
AU  - Zhen N
AD  - 2 Department of Clinical Laboratory Medicine, Shanghai Tenth People's Hospital of
      Tongji University, Shanghai, China.
FAU - Li, Ning
AU  - Li N
AD  - 3 Central Laboratory, Shanghai Municipal Hospital of Traditional Chinese
      Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
FAU - Li, Yan
AU  - Li Y
AD  - 1 Department of Oncology, Shanghai Municipal Hospital of Traditional Chinese
      Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
FAU - Li, Yong-Xin
AU  - Li YX
AD  - 1 Department of Oncology, Shanghai Municipal Hospital of Traditional Chinese
      Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
AD  - 3 Central Laboratory, Shanghai Municipal Hospital of Traditional Chinese
      Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Tumour Biol
JT  - Tumour biology : the journal of the International Society for Oncodevelopmental
      Biology and Medicine
JID - 8409922
RN  - 0 (ATG13 protein, human)
RN  - 0 (Adaptor Proteins, Signal Transducing)
RN  - 0 (Antigens, Neoplasm)
RN  - 0 (Autophagy-Related Proteins)
RN  - 0 (Intracellular Signaling Peptides and Proteins)
RN  - 0 (MAGED1 protein, human)
RN  - 0 (Neoplasm Proteins)
RN  - 0 (RNA, Small Interfering)
RN  - EC 2.7.11.1 (AMP-Activated Protein Kinases)
RN  - EC 2.7.11.1 (Autophagy-Related Protein-1 Homolog)
RN  - EC 2.7.11.1 (ULK1 protein, human)
SB  - IM
MH  - A549 Cells
MH  - AMP-Activated Protein Kinases/biosynthesis/*genetics
MH  - Adaptor Proteins, Signal Transducing/biosynthesis/*genetics
MH  - Antigens, Neoplasm/*genetics
MH  - Autophagy/genetics
MH  - Autophagy-Related Protein-1 Homolog/biosynthesis/*genetics
MH  - Autophagy-Related Proteins/biosynthesis/*genetics
MH  - Carcinoma, Non-Small-Cell Lung/*genetics/pathology
MH  - Gene Expression Regulation, Neoplastic
MH  - Humans
MH  - Intracellular Signaling Peptides and Proteins/biosynthesis/*genetics
MH  - Neoplasm Proteins/antagonists & inhibitors/*genetics
MH  - Phosphorylation
MH  - RNA, Small Interfering
MH  - Signal Transduction
OTO - NOTNLM
OT  - AMPK/Ulk1/Atg13 signaling pathway
OT  - NRAGE
OT  - autophagy
OT  - non-small-cell lung cancer
OT  - proliferation
EDAT- 2017/06/24 06:00
MHDA- 2017/07/14 06:00
CRDT- 2017/06/23 06:00
AID - 10.1177/1010428317709676 [doi]
PST - ppublish
SO  - Tumour Biol. 2017 Jun;39(6):1010428317709676. doi: 10.1177/1010428317709676.