Evidence map›Paper›PMID 31412953›Full record

ArticleJournal of experimental & clinical cancer research : CR2019

Tubeimoside-I sensitizes colorectal cancer cells to chemotherapy by inducing ROS-mediated impaired autophagolysosomes accumulation.

Jianghong Yan, Xiaoyun Dou, Jing Zhou, Yuanfeng Xiong, Ling Mo, Longhao Li, Yunlong Lei

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

29 citing papers in PubMed, 48 citations in OpenAlex.

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  19. Chinese endemic medicinal plantFrontiers in pharmacology · 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.

Jianghong YanInstitute of Life Science,Chongqing Medical University, Chongqing, 400016, China.
Xiaoyun DouInstitute of Life Science,Chongqing Medical University, Chongqing, 400016, China.
Jing ZhouDepartment of Biochemistry and Molecular Biology and Molecular Medicine and Cancer Research Center, Chongqing Medical University, Chongqing, 400016, People's Republic of China.
Yuanfeng XiongDepartment of Medical Laboratory Technology, Chongqing Medical University, Chongqing, 400016, China.
Ling MoDepartment of Medical Laboratory Technology, Chongqing Medical University, Chongqing, 400016, China.
Longhao LiDepartment of Oncology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China. llh@hospital.cqmu.edu.cn.
Yunlong LeiDepartment of Biochemistry and Molecular Biology and Molecular Medicine and Cancer Research Center, Chongqing Medical University, Chongqing, 400016, People's Republic of China. leiyunglong@cqmu.edu.cn.
Chongqing Medical University · CNFirst Affiliated Hospital of Chongqing Medical University · CN

Funding

Chinese NSFC 31400999Chinese NSFC 81872014
6 · The paper itself

Abstract

backgroundTubeimoside-I (TBM), a plant-derived bioactive compound, shows antitumor activity in different tumors and can enhance the efficacy of chemotherapeutic agents. However, the detail mechanism underlying remains to be elucidated.

methodsThe cytotoxic potential of TBM towards CRC cells was examined by CCK8 assay, colony formation, LDH release assay, flow cytometry method and Western blots. The ROS levels, autophagy, apoptosis, chemosensitivity to 5-FU or DOX, etc. were determined between control and TBM-treated CRC cells.

resultsIn this study, we found that TBM could inhibit proliferation and induce apoptosis in colorectal cancer (CRC) cells. Intriguingly, TBM treatment could either promote autophagy initiation by ROS-induced AMPK activation, or block autophagy flux through inhibiting lysosomal hydrolytic enzymes, which leaded to massive impaired autophagylysosomes accumulation. Administration of autophagy initiation inhibitor (3-MA or selective ablation of autophagy related proteins) relieves TBM-induced CRC suppression, while combination use of autophagy flux inhibitor chloroquine (CQ) slightly augments TBM-induced cell death, suggesting that impaired autophagylysosomes accumulation contributes to TBM-induced growth inhibition in CRC cells. Notably, as an autophagy flux inhibitor, TBM works synergistically with 5-fluorouracil (5-FU) or doxorubicin (DOX) in CRC suppression.

conclusionTogether, our study provides new insights regarding the anti-tumor activity of TBM against CRC, and established potential applications of TBM for CRC combination therapies in clinic.

Indexed as

Antineoplastic AgentsApoptosisAutophagyCell Line, TumorCell SurvivalDrug Resistance, NeoplasmDrugs, Chinese HerbalDrug SynergismFluorouracilHumansLysosomesPhagosomesProteolysisReactive Oxygen SpeciesSaponinsSignal TransductionAntineoplastic AgentsDrugs, Chinese HerbalFluorouracilReactive Oxygen SpeciesSaponinsTriterpenestubeimoside IAMPKAutophagyChemosensitivityROSTubeimoside-I

Identifiers

PMID31412953
PMCPMC6694658
OpenAlexW2968806891

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.