Evidence map›Paper›PMID 31186406›Full record

ArticleCell death & disease2019

Autophagic flux disruption contributes to Ganoderma lucidum polysaccharide-induced apoptosis in human colorectal cancer cells via MAPK/ERK activation.

Haitao Pan, Yujie Wang, Kun Na, Ying Wang, Lu Wang, Zhenhao Li, Chengjie Guo, Dandan Guo, Xingya Wang

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
12.1field-weighted citation impact, top 1% 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

68 citing papers in PubMed, 160 citations in OpenAlex.

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  18. Blockage of Autophagy for Cancer Therapy: A Comprehensive Review.International journal of molecular sciences · 2024
    Review
  19. Review
  20. Article

8 more citing papers are in PubMed but not listed here.

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

9 authors at 1 institution in 1 country.

Haitao PanDepartment of Pharmaceutical Science, Zhejiang Chinese Medical University, 548 Binwen Road, 310053, Hangzhou, Zhejiang, China.
Yujie WangDepartment of Pharmaceutical Science, Zhejiang Chinese Medical University, 548 Binwen Road, 310053, Hangzhou, Zhejiang, China.
Kun NaDepartment of Pharmaceutical Science, Zhejiang Chinese Medical University, 548 Binwen Road, 310053, Hangzhou, Zhejiang, China.
Ying WangDepartment of Pharmaceutical Science, Zhejiang Chinese Medical University, 548 Binwen Road, 310053, Hangzhou, Zhejiang, China.
Lu WangDepartment of Pharmaceutical Science, Zhejiang Chinese Medical University, 548 Binwen Road, 310053, Hangzhou, Zhejiang, China.
Zhenhao LiZhejiang Shouxiangu Institute of Rare Medicine Plant, 12, Huanglong 3rd Road, 321200, Wuyi, Zhejiang, China.
Chengjie GuoDepartment of Pharmaceutical Science, Zhejiang Chinese Medical University, 548 Binwen Road, 310053, Hangzhou, Zhejiang, China.
Dandan GuoDepartment of Pharmaceutical Science, Zhejiang Chinese Medical University, 548 Binwen Road, 310053, Hangzhou, Zhejiang, China.
Xingya WangDepartment of Pharmaceutical Science, Zhejiang Chinese Medical University, 548 Binwen Road, 310053, Hangzhou, Zhejiang, China. xywang@zcmu.edu.cn.ORCID http://orcid.org/0000-0001-6986-3240
Zhejiang Chinese Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Targeting autophagy may serve as a promising strategy for cancer therapy. Ganoderma lucidum polysaccharide (GLP) has been shown to exert promising anti-cancer effects. However, the underlying mechanisms remain elusive. Whether GLP regulates autophagy in cancer has never been reported. In this study, GLP induced the initiation of autophagy in colorectal cancer (CRC) HT-29 and HCT116 cells, as evidenced by enhanced level of LC3-II protein, GFP-LC3 puncta, and increased formation of double membrane vacuoles. However, GLP treatment caused marked increase of p62 expression. Addition of late stage autophagy inhibitor, chloroquine (CQ), further enhanced LC3-II and p62 level, as well as increased autophagosome accumulation, suggesting a blockage of autophagic flux by GLP in CRC cells. We then found GLP blocked autophagosome and lysosome fusion as determined by mRFP-GFP-LC3 colocalization analysis. Mechanistic study revealed that GLP-induced disruption of autophagosome-lysosome fusion is due to reduced lysosome acidification and lysosomal cathepsin activities. Cell viability and flow cytometry assays revealed that GLP-induced autophagosome accumulation is responsible for GLP-induced apoptosis in CRC cells. In line with this, inhibition of autophagy initiation by 3-methyladenine (3-MA), an early stage autophagy inhibitor, attenuated GLP-induced apoptosis. In contrast, suppression of autophagy at late stage by CQ enhanced the anti-cancer effect of GLP. Furthermore, we demonstrated that GLP-induced autophagosome accumulation and apoptosis is mediated via MAPK/ERK activation. Finally, GLP inhibited tumor growth and also inhibited autophagic flux in vivo. These results unveil new molecular mechanism underlying anti-cancer effects of GLP, suggesting that GLP is a potent autophagy inhibitor and might be useful in anticancer therapy.

Indexed as

ReishiAnimalsAntineoplastic AgentsApoptosisAutophagosomesAutophagyCell SurvivalChloroquineColorectal NeoplasmsHCT116 CellsHT29 CellsHumansLysosomesMaleMAP Kinase Signaling SystemMiceAntineoplastic AgentsChloroquineMap1lc3b protein, mouseMicrotubule-Associated ProteinsMitogen-Activated Protein Kinase KinasesP62 protein, humanPolysaccharidesRNA-Binding Proteins

Identifiers

PMID31186406
PMCPMC6560101
OpenAlexW2950274560

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.