Evidence map›Paper›PMID 31871431›Full record

ArticleCancer cell international2019

Blocking AMPK/ULK1-dependent autophagy promoted apoptosis and suppressed colon cancer growth.

Jing Liu, Shuaiyu Long, Huanan Wang, Nannan Liu, Chuchu Zhang, Lingling Zhang, Yingjie Zhang

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
5.9field-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

33 citing papers in PubMed, 61 citations in OpenAlex.

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  17. Sestrin2 in cancer: a foe or a friend?Biomarker research · 2022
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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 2 institutions in 1 country.

Jing Liu *1College of Biology, Hunan University, Changsha, 410082 China.
Shuaiyu Long *1College of Biology, Hunan University, Changsha, 410082 China.
Huanan Wang2Department of Laboratory Medicine, The Third Xiangya Hospital, Central South University, Changsha, 410013 China.
Nannan Liu1College of Biology, Hunan University, Changsha, 410082 China.
Chuchu Zhang1College of Biology, Hunan University, Changsha, 410082 China.
Lingling Zhang2Department of Laboratory Medicine, The Third Xiangya Hospital, Central South University, Changsha, 410013 China.
Yingjie Zhang1College of Biology, Hunan University, Changsha, 410082 China.ORCID 0000-0002-9207-2364
Hunan University · CNCentral South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAutophagy is an evolutionarily conserved process through which cells degrade and recycle cytoplasm. The relation among autophagy, apoptosis and tumor is highly controversial until now and the molecular mechanism is poorly understood.

methodsCell viability and apoptosis were detected by CCK8, crystal violet staining, Hoechst333342 staining and flow cytometry. The expression of AMPK and ULK1 was analyzed by western blotting. Colon cancer growth suppression by NVP-BEZ235 or CQ in vivo was studied in a tumor xenograft mouse model.

resultsOur previous study revealed that NVP-BEZ235 suppressed colorectal cancer growth via inducing apoptosis, however later, we found it also initiated autophagy simultaneously. In this present study, our results show that NVP-BEZ235 induced autophagy through AMPK/ULK1 pathway in colon cancer cells. Blocking autophagy by knocking down AMPK or ULK1 inhibited cell proliferation and further promoted NVP-BEZ235 induced apoptosis. Meantime, the autophagy inhibitor chloroquine (CQ) shows obvious effect on inhibiting cell proliferation but not on inducing apoptosis, while it significantly increased NVP-BEZ235 induced apoptosis. Furthermore, the combinational therapy of NVP-BEZ235 and CQ shows synergistic antitumor effects in colon cancer in vivo.

conclusionNVP-BEZ235 induced AMPK/ULK1-dependent autophagy. Targeting this autophagy suppressed colon cancer growth through further promoting apoptosis, which is a potential therapeutic option for clinical patients.

Indexed as

ApoptosisAutophagyColon cancerCQNVP-BEZ235

Identifiers

PMID31871431
PMCPMC6911288
OpenAlexW2995242031

What OpenQuestion holds

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Registered trials

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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.