Evidence map›Paper›PMID 41809875›Full record

ArticleWorld journal of gastroenterology2026

Wogonin derivative V8 enhances bortezomib efficacy in gastric carcinoma by disrupting lysosome-mediated drug resistance.

Si-Chan Li, Shun-Zi Shao, Yu-Hang Zhang, Yu Zhou, Wen-Tao Shang, Yuan Gao, Qi-Bin He, Qing-Long Guo, Chuan-Yong Guo, Xiao-Bo Zhang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in World journal of gastroenterology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

10 authors.

Si-Chan LiJiangsu Key Laboratory of Carcinogenesis and Intervention, School of Basic Medicine and Clinical Pharmacy, China Pharmaceutical University, Nanjing 210009, Jiangsu Province, China.
Shun-Zi ShaoDepartment of Gastroenterology, Jiangning Hospital, Nanjing Medical University, Nanjing 211199, Jiangsu Province, China.
Yu-Hang ZhangJiangsu Key Laboratory of Carcinogenesis and Intervention, School of Basic Medicine and Clinical Pharmacy, China Pharmaceutical University, Nanjing 210009, Jiangsu Province, China.
Yu ZhouJiangsu Key Laboratory of Carcinogenesis and Intervention, School of Basic Medicine and Clinical Pharmacy, China Pharmaceutical University, Nanjing 210009, Jiangsu Province, China.
Wen-Tao ShangJiangsu Key Laboratory of Carcinogenesis and Intervention, School of Basic Medicine and Clinical Pharmacy, China Pharmaceutical University, Nanjing 210009, Jiangsu Province, China.
Yuan GaoPharmaceutical Animal Experimental Center, China Pharmaceutical University, Nanjing 211198, Jiangsu Province, China.
Qi-Bin HeDepartment of Gastroenterology, Jiangning Hospital, Nanjing Medical University, Nanjing 211199, Jiangsu Province, China.
Qing-Long GuoJiangsu Key Laboratory of Carcinogenesis and Intervention, School of Basic Medicine and Clinical Pharmacy, China Pharmaceutical University, Nanjing 210009, Jiangsu Province, China.
Chuan-Yong GuoDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Nanjing Medical University, Shanghai 200072, China.
Xiao-Bo ZhangJiangsu Key Laboratory of Carcinogenesis and Intervention, School of Basic Medicine and Clinical Pharmacy, China Pharmaceutical University, Nanjing 210009, Jiangsu Province, China. xiaobozhangxibo@126.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBortezomib (BTZ) is ineffective in gastric carcinoma (GC) due to lysosome-mediated resistance. Wogonin derivative V8 targets lysosomes.

aimTo address the limited efficacy of BTZ in GC and explore whether wogonin derivative V8 enhances anti-GC effects by overcoming lysosome-mediated resistance.

methods

resultsBTZ was trapped in GC cell lysosomes, reducing its proteasome accessibility and inducing resistance; lysosome number correlated positively with the half-maximal inhibitory concentration of BTZ. V8 induced lysosomal damage/deacidification, increasing intracellular BTZ availability. V8 + BTZ synergistically inhibited GC cell growth (CI < 1), upregulated proteotoxic stress markers (

conclusionLysosomes mediate BTZ resistance in GC; V8 overcomes this by disrupting lysosomes, enabling BTZ to target proteasomes. V8 + BTZ is a safe, effective strategy against GC.

Indexed as

Antineoplastic Combined Chemotherapy ProtocolsBortezomibDrug Resistance, NeoplasmFlavanonesLysosomesStomach NeoplasmsAnimalsAutophagyBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsCell Line, TumorCell SurvivalDrug SynergismHumansMiceMice, NudeXenograft Model Antitumor AssaysBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsBortezomibFlavanonesTFEB protein, humanwogoninBortezomibDrug resistanceGastric carcinomaLysosomePatient-derived organoidsTranscription factor EBWogonin derivative V8

Identifiers

PMID41809875
PMCPMC12968567

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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.