Evidence map›Paper›PMID 28103582›Full record

ArticleOncotarget2017

AMPK-autophagy inhibition sensitizes icaritin-induced anti-colorectal cancer cell activity.

Chunxian Zhou, Jun Gu, Gang Zhang, Da Dong, Qunying Yang, Min-Bin Chen, Dongfeng Xu

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
5.2field-weighted citation impact, top 5% 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

20 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
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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 4 institutions in 1 country.

Chunxian ZhouDepartment of Interventional Radiology, Wujiang Hospital Affiliated to Nantong University, Wujiang, Suzhou, China.
Jun GuThe Department of Orthopedics, The Second Affiliated Hospital of Soochow University, Suzhou, China.
Gang ZhangDepartment of Interventional Radiology, Wujiang Hospital Affiliated to Nantong University, Wujiang, Suzhou, China.
Da DongDepartment of Interventional Radiology, Wujiang Hospital Affiliated to Nantong University, Wujiang, Suzhou, China.
Qunying YangDepartment of Interventional Radiology, Wujiang Hospital Affiliated to Nantong University, Wujiang, Suzhou, China.
Min-Bin ChenDepartment of Oncology, Kunshan First People's Hospital Affiliated to Jiangsu University, Kunshan, 215300, China.
Dongfeng XuDepartment of Interventional Radiology, Wujiang Hospital Affiliated to Nantong University, Wujiang, Suzhou, China.
Nantong University · CNWujiang District People's Hospital · CNJiangsu University · CNSecond Affiliated Hospital of Soochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The current research studied the potential effect of autophagy on icaritin-induced anti-colorectal cancer (CRC) cell activity. Treatment of icaritin in both primary and established (HT-29) CRC cells induced feedback activation of autophagy, evidenced by p62 degradation, Beclin-1 and autophagy-related gene-5 (ATG-5) upregulation, as well as light chain 3B (LC3B)-GFP puncta formation. Pharmacological inhibiting of autophagy dramatically potentiated icaritin-induced CRC cell death and apoptosis. Meanwhile, shRNA-mediated knockdown of Beclin-1 or ATG-5 also sensitized icaritin-induced CRC cell death and apoptosis. Icaritin activated AMP-activated protein kinase (AMPK) signaling in CRC cells, functioning as the upstream signaling for autophagy activation. shRNA/siRNA-mediated knockdown of AMPKα1inhibited icaritin-induced autophagy activation, but exacerbated CRC cell death. On the other hand, the AMPK activator compound 13 (C13) or the autophagy activator MHY1485 attenuated icaritin-induced cytotoxicity. In nude mice, icaritin (oral administration)-induced HT-29 tumor growth inhibition was potentiated when combined with AMPKα1 shRNA knockdown in tumors. We conclude that feedback activation of AMPK-autophagy pathway could be a primary resistance factor of icaritin.

Indexed as

AMP-Activated Protein KinasesAnimalsApoptosisAutophagyAutophagy-Related Protein 5Beclin-1Blotting, WesternCell SurvivalColorectal NeoplasmsFlavonoidsHT29 CellsHumansMaleMice, NudeMiddle AgedMorpholines4,6-dimorpholino-N-(4-nitrophenyl)-1,3,5-triazin-2-amineAMP-Activated Protein KinasesAutophagy-Related Protein 5Beclin-1FlavonoidsicaritinMorpholinesTriazinesAMPKautophagychemosensitizationcolorectal cancericaritin

Identifiers

PMID28103582
PMCPMC5362439
OpenAlexW2571834185

What OpenQuestion holds

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LicenceCC BY
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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.