Evidence map›Paper›PMID 26876613›Full record

ArticleCellular signalling2016

Inhibition of mTOR by apigenin in UVB-irradiated keratinocytes: A new implication of skin cancer prevention.

Bryan B Bridgeman, Pu Wang, Boping Ye, Jill C Pelling, Olga V Volpert, Xin Tong

Open access · greenAbstract read
In one paragraph

Article in Cellular signalling, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
6.3field-weighted citation impact, top 3% 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

38 citing papers in PubMed, 96 citations in OpenAlex.

  1. Review
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  13. Flavonoids and their therapeutic applications in skin diseases.Archives of dermatological research · 2023
    Review
  14. Article
  15. Article
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  18. The Role of Probiotics in Skin Photoaging and Related Mechanisms: A Review.Clinical, cosmetic and investigational dermatology · 2022
    Review
  19. Review
  20. Flavonoids in Skin Senescence Prevention and Treatment.International journal of molecular sciences · 2021
    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

6 authors at 2 institutions in 2 countries.

Bryan B Bridgeman *Department of Pathology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.
Pu Wang *School of Life Sciences and Technology, China Pharmaceutical University, Nanjing 210009, PR China.
Boping YeSchool of Life Sciences and Technology, China Pharmaceutical University, Nanjing 210009, PR China.
Jill C PellingDepartment of Pathology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.
Olga V VolpertDepartment of Urology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.
Xin TongDepartment of Pathology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.
Northwestern University · USChina Pharmaceutical University · CN

Funding

Tumor Environment and Metastasis (TEAM) Research ProgramP30CA060553 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Daniela E Matei · 1993 to 2026
$153.9M
Apigenin restores TSP-1 expression in UVB-irradiated keratinocytesR01CA172669 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI VOLPERT, OLGA VALERY · 2013 to 2017
$2.3M
AMPK as a molecular target for chemoprevention by apigenin in preneoplastic skinR21CA161181 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI TONG, XIN · 2012 to 2013
$358k
NCI NIH HHS CA161181NCI NIH HHS CA172669NCI NIH HHS P30 CA060553NCI NIH HHS R01 CA172669NCI NIH HHS R21 CA161181
6 · The paper itself

Abstract

Ultraviolet B (UVB) radiation is the major environmental risk factor for developing skin cancer, the most common cancer worldwide, which is characterized by aberrant activation of Akt/mTOR (mammalian target of rapamycin). Importantly, the link between UV irradiation and mTOR signaling has not been fully established. Apigenin is a naturally occurring flavonoid that has been shown to inhibit UV-induced skin cancer. Previously, we have demonstrated that apigenin activates AMP-activated protein kinase (AMPK), which leads to suppression of basal mTOR activity in cultured keratinocytes. Here, we demonstrated that apigenin inhibited UVB-induced mTOR activation, cell proliferation and cell cycle progression in mouse skin and in mouse epidermal keratinocytes. Interestingly, UVB induced mTOR signaling via PI3K/Akt pathway, however, the inhibition of UVB-induced mTOR signaling by apigenin was not Akt-dependent. Instead, it was driven by AMPK activation. In addition, mTOR inhibition by apigenin in keratinocytes enhanced autophagy, which was responsible, at least in part, for the decreased proliferation in keratinocytes. In contrast, apigenin did not alter UVB-induced apoptosis. Taken together, our results indicate the important role of mTOR inhibition in UVB protection by apigenin, and provide a new target and strategy for better prevention of UV-induced skin cancer.

Indexed as

Ultraviolet RaysAMP-Activated Protein KinasesAnimalsAnticarcinogenic AgentsApigeninApoptosisAutophagyCell CycleCell LineCell ProliferationKeratinocytesMice, Inbred BALB CPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionSkin NeoplasmsAMP-Activated Protein KinasesAnticarcinogenic AgentsApigeninPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesAktAMPKApigeninAutophagymTORUVB

Identifiers

PMID26876613
PMCPMC4788564
OpenAlexW2259840879

What OpenQuestion holds

Textmetadata
LicenceTDM
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.