Evidence map›Paper›PMID 26656173›Full record

ArticlePloS one2015

Anti-Tumor Activity of Yuanhuacine by Regulating AMPK/mTOR Signaling Pathway and Actin Cytoskeleton Organization in Non-Small Cell Lung Cancer Cells.

Ji In Kang, Ji-Young Hong, Hye-Jung Lee, Song Yi Bae, Cholomi Jung, Hyen Joo Park, Sang Kook Lee

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 2 pooled it
1.4field-weighted citation impact, top 19% 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

31 citing papers in PubMed, 2 syntheses or guidelines pooled it, 54 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  13. AMPK suppresses Th2 cell responses by repressing mTORC2.Experimental & molecular medicine · 2022
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  14. Review
  15. Review
  16. Article
  17. Article
  18. Daphnane-type diterpenes from genusChinese herbal medicines · 2021
    Review
  19. Article
  20. Article
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

7 authors at 1 institution in 1 country.

Ji In KangCollege of Pharmacy, Seoul National University, Seoul, 151-742, Republic of Korea.
Ji-Young HongCollege of Pharmacy, Seoul National University, Seoul, 151-742, Republic of Korea.
Hye-Jung LeeCollege of Pharmacy, Seoul National University, Seoul, 151-742, Republic of Korea.
Song Yi BaeCollege of Pharmacy, Seoul National University, Seoul, 151-742, Republic of Korea.
Cholomi JungCollege of Pharmacy, Seoul National University, Seoul, 151-742, Republic of Korea.
Hyen Joo ParkCollege of Pharmacy, Seoul National University, Seoul, 151-742, Republic of Korea.
Sang Kook LeeCollege of Pharmacy, Seoul National University, Seoul, 151-742, Republic of Korea.
Seoul National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Yuanhuacine (YC), a daphnane diterpenoid from the flowers of Daphne genkwa, exhibited a potential growth inhibitory activity against human non-small cell lung cancer (NSCLC) cells. YC also suppressed the invasion and migration of lung cancer cells. However, the precise molecular mechanisms remain to be elucidated. In the present study, we report that YC significantly activated AMP-activated protein kinase (AMPK) signaling pathway and suppressed mTORC2-mediated downstream signaling pathway in H1993 human NSCLC cells. AMPK plays an important role in energy metabolism and cancer biology. Therefore, activators of AMPK signaling pathways can be applicable to the treatment of cancer. YC enhanced the expression of p-AMPKα. The co-treatment of YC and compound C (an AMPK inhibitor) or metformin (an AMPK activator) also confirmed that YC increases p-AMPKα. YC also suppressed the activation of the mammalian target of rapamycin (mTOR) expression, a downstream target of AMPK. Further study revealed that YC modulates mTORC2-associated downstream signaling pathways with a decreased expressions of p-Akt, p-protein kinase C alpha (PKCα), p-ras-related C3 botulinum toxin substrate 1 (Rac1) and filamentous actin (F-actin) that are known to activate cell growth and organize actin cytoskeleton. In addition, YC inhibited the tumor growth in H1993 cell-implanted xenograft nude mouse model. These data suggest the YC could be a potential candidate for cancer chemotherapeutic agents derived from natural products by regulating AMPK/mTORC2 signaling pathway and actin cytoskeleton organization.

Indexed as

Actin CytoskeletonAMP-Activated Protein KinasesAnimalsAntineoplastic AgentsBiomarkers, TumorCarcinoma, Non-Small-Cell LungCell Line, TumorCell MovementCell ProliferationDiterpenesFemaleGefitinibHumansLung NeoplasmsMice, Inbred BALB CMice, NudeAMP-Activated Protein KinasesAntineoplastic AgentsBiomarkers, TumorDiterpenesGefitinibQuinazolinesSirolimusTOR Serine-Threonine KinasesYuanhuacin

Identifiers

PMID26656173
PMCPMC4676678
OpenAlexW2191089917

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.