Evidence map›Paper›PMID 33838688›Full record

ArticleJournal of experimental & clinical cancer research : CR2021

Dehydrodiisoeugenol inhibits colorectal cancer growth by endoplasmic reticulum stress-induced autophagic pathways.

Changhong Li, Kui Zhang, Guangzhao Pan, Haoyan Ji, Chongyang Li, Xiaowen Wang, Xin Hu, Ruochen Liu, Longfei Deng, Yi Wang and 2 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
16.3field-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

38 citing papers in PubMed, 98 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 2 institutions in 1 country.

Changhong Li *State Key Laboratory of Silkworm Genome Biology, College of Sericulture, Textile and Biomass sciences, Southwest University, #2, Tiansheng Rd., Beibei District, Chongqing, 400716, China.
Kui Zhang *State Key Laboratory of Silkworm Genome Biology, College of Sericulture, Textile and Biomass sciences, Southwest University, #2, Tiansheng Rd., Beibei District, Chongqing, 400716, China.
Guangzhao PanState Key Laboratory of Silkworm Genome Biology, College of Sericulture, Textile and Biomass sciences, Southwest University, #2, Tiansheng Rd., Beibei District, Chongqing, 400716, China.
Haoyan JiState Key Laboratory of Silkworm Genome Biology, College of Sericulture, Textile and Biomass sciences, Southwest University, #2, Tiansheng Rd., Beibei District, Chongqing, 400716, China.
Chongyang LiState Key Laboratory of Silkworm Genome Biology, College of Sericulture, Textile and Biomass sciences, Southwest University, #2, Tiansheng Rd., Beibei District, Chongqing, 400716, China.
Xiaowen WangState Key Laboratory of Silkworm Genome Biology, College of Sericulture, Textile and Biomass sciences, Southwest University, #2, Tiansheng Rd., Beibei District, Chongqing, 400716, China.
Xin HuState Key Laboratory of Silkworm Genome Biology, College of Sericulture, Textile and Biomass sciences, Southwest University, #2, Tiansheng Rd., Beibei District, Chongqing, 400716, China.
Ruochen LiuState Key Laboratory of Silkworm Genome Biology, College of Sericulture, Textile and Biomass sciences, Southwest University, #2, Tiansheng Rd., Beibei District, Chongqing, 400716, China.
Longfei DengState Key Laboratory of Silkworm Genome Biology, College of Sericulture, Textile and Biomass sciences, Southwest University, #2, Tiansheng Rd., Beibei District, Chongqing, 400716, China.
Yi WangAffiliated Hospital of Southwest University (the Ninth People's Hospital of Chongqing), Chongqing, 400716, China.
Liqun YangState Key Laboratory of Silkworm Genome Biology, College of Sericulture, Textile and Biomass sciences, Southwest University, #2, Tiansheng Rd., Beibei District, Chongqing, 400716, China. cysylq@swu.edu.cn.
Hongjuan CuiState Key Laboratory of Silkworm Genome Biology, College of Sericulture, Textile and Biomass sciences, Southwest University, #2, Tiansheng Rd., Beibei District, Chongqing, 400716, China.
Southwest University · CNState Key Laboratory of Silkworm Genomic Biology

Funding

Chongqing Natural Science foundation of Chongqing cstc2019jcyj-zdxmX0033Chongqing University Innovation Team Building Program funded projects CXTDX201601010the China Postdoctoral Science Foundation 2017M620408the China Postdoctoral Science Foundation 2019T120801the Fundamental Research Funds for the Central Universities XDJK2019C089the National Key Research and Development Program of China 2016YFC1302204the National Key Research and Development Program of China 2017YFC1308601the National Natural Science Foundation of China 31672496the National Natural Science Foundation of China 31802142the National Natural Science Foundation of China 81672502the National Natural Science Foundation of China 81872071
6 · The paper itself

Abstract

backgroundDehydrodiisoeugenol (DEH), a novel lignan component extracted from nutmeg, which is the seed of Myristica fragrans Houtt, displays noticeable anti-inflammatory and anti-allergic effects in digestive system diseases. However, the mechanism of its anticancer activity in gastrointestinal cancer remains to be investigated.

methodsIn this study, the anticancer effect of DEH on human colorectal cancer and its underlying mechanism were evaluated. Assays including MTT, EdU, Plate clone formation, Soft agar, Flow cytometry, Electron microscopy, Immunofluorescence and Western blotting were used in vitro. The CDX and PDX tumor xenograft models were used in vivo.

resultsOur findings indicated that treatment with DEH arrested the cell cycle of colorectal cancer cells at the G1/S phase, leading to significant inhibition in cell growth. Moreover, DEH induced strong cellular autophagy, which could be inhibited through autophagic inhibitors, with a rction in the DEH-induced inhibition of cell growth in colorectal cancer cells. Further analysis indicated that DEH also induced endoplasmic reticulum (ER) stress and subsequently stimulated autophagy through the activation of PERK/eIF2α and IRE1α/XBP-1 s/CHOP pathways. Knockdown of PERK or IRE1α significantly decreased DEH-induced autophagy and retrieved cell viability in cells treated with DEH. Furthermore, DEH also exhibited significant anticancer activities in the CDX- and PDX-models.

conclusionsCollectively, our studies strongly suggest that DEH might be a potential anticancer agent against colorectal cancer by activating ER stress-induced inhibition of autophagy.

Indexed as

AnimalsAutophagyColorectal NeoplasmsEndoplasmic Reticulum StressEugenolFemaleHumansMiceMice, Inbred NODdehydrodiisoeugenolEugenolAnticancer agentAutophagy inhibitionColorectal cancerDehydrodiisoeugenol (DEH)Endoplasmic reticulum (ER) stress

Identifiers

PMID33838688
PMCPMC8035743
OpenAlexW3153216022

What OpenQuestion holds

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LicenceCC BY
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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.