Evidence map›Paper›PMID 28765579›Full record

ArticleScientific reports2017

Inhibition of AKT1 signaling promotes invasion and metastasis of non-small cell lung cancer cells with K-RAS or EGFR mutations.

Guanhua Rao, Mariaelena Pierobon, In-Kyu Kim, Wei-Hsun Hsu, Jianghong Deng, Yong-Wha Moon, Emanuel F Petricoin, Yu-Wen Zhang, Yisong Wang, Giuseppe Giaccone

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
3.5field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

54 citing papers in PubMed, 102 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. [Inhibitory effect ofNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025
    Article
  7. Review
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  11. Article
  12. Article
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  15. Review
  16. Article
  17. Centipeda minima active components and mechanisms in lung cancer.BMC complementary medicine and therapies · 2023
    Article
  18. Article
  19. LAFITE Reveals the Complexity of Transcript Isoforms in Subcellular Fractions.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 1 country.

Guanhua RaoLombardi Comprehensive Cancer Center, Georgetown University, Washington, DC, USA.
Mariaelena PierobonCenter for Applied Proteomics and Molecular Medicine, George Mason University, Manassas, VA, USA.
In-Kyu KimLombardi Comprehensive Cancer Center, Georgetown University, Washington, DC, USA.
Wei-Hsun HsuLombardi Comprehensive Cancer Center, Georgetown University, Washington, DC, USA.
Jianghong DengCenter for Applied Proteomics and Molecular Medicine, George Mason University, Manassas, VA, USA.
Yong-Wha MoonLombardi Comprehensive Cancer Center, Georgetown University, Washington, DC, USA.
Emanuel F PetricoinCenter for Applied Proteomics and Molecular Medicine, George Mason University, Manassas, VA, USA.
Yu-Wen ZhangLombardi Comprehensive Cancer Center, Georgetown University, Washington, DC, USA.
Yisong WangLombardi Comprehensive Cancer Center, Georgetown University, Washington, DC, USA.
Giuseppe GiacconeLombardi Comprehensive Cancer Center, Georgetown University, Washington, DC, USA. gg496@georgetown.edu.
Georgetown University Medical Center · USGeorge Mason University · USGeorgetown University · US

Funding

Tissue Culture Shared ResourceP30CA051008 · NCI · GEORGETOWN UNIVERSITY · PI Louis M Weiner · 1990 to 2026
$71.5M
NCI NIH HHS P30 CA051008
6 · The paper itself

Abstract

Accumulating evidence supports a role of the PI3K-AKT pathway in the regulation of cell motility, invasion and metastasis. AKT activation is known to promote metastasis, however under certain circumstances, it also shows an inhibitory activity on metastatic processes, and the cause of such conflicting results is largely unclear. Here we found that AKT1 is an important regulator of metastasis and down-regulation of its activity is associated with increased metastatic potential of A549 cells. Inhibition of AKT1 enhanced migration and invasion in KRAS- or EGFR-mutant non-small cell lung cancer (NSCLC) cells. The allosteric AKT inhibitor MK-2206 promoted metastasis of KRAS-mutated A549 cells in vivo. We next identified that the phosphorylation of Myristoylated alanine-rich C-kinase substrate (MARCKS) and LAMC2 protein level were increased with AKT1 inhibition, and MARCKS or LAMC2 knockdown abrogated migration and invasion induced by AKT1 inhibition. This study unravels an anti-metastatic role of AKT1 in the NSCLC cells with KRAS or EGFR mutations, and establishes an AKT1-MARCKS-LAMC2 feedback loop in this regulation.

Indexed as

Cell MovementA549 CellsCarcinoma, Non-Small-Cell LungEnzyme InhibitorsErbB ReceptorsHeterocyclic Compounds, 3-RingHumansLamininModels, BiologicalMutationMyristoylated Alanine-Rich C Kinase SubstrateProto-Oncogene Proteins c-aktProto-Oncogene Proteins p21(ras)Signal TransductionAKT1 protein, humanEGFR protein, humanEnzyme InhibitorsErbB ReceptorsHeterocyclic Compounds, 3-RingKRAS protein, humanLAMC2 protein, humanLamininMARCKS protein, humanMK 2206Myristoylated Alanine-Rich C Kinase SubstrateProto-Oncogene Proteins c-aktProto-Oncogene Proteins p21(ras)

Identifiers

PMID28765579
PMCPMC5539338
OpenAlexW2738377689

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.