Evidence map›Paper›PMID 39392399›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2024

Gastric Cancer Actively Remodels Mechanical Microenvironment to Promote Chemotherapy Resistance via MSCs-Mediated Mitochondrial Transfer.

Xin He, Li Zhong, Nan Wang, Baiwei Zhao, Yannan Wang, Xinxiang Wu, Changyu Zheng, Yueheng Ruan, Jianfeng Hou, Yusheng Luo and 4 more

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
–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

32 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  19. Mitochondria transfer in tissue homeostasis and diseases.International journal of biological sciences · 2026
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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

14 authors.

Xin HeScientific Research Center, The Seventh Affiliated Hospital of Sun Yat-sen University, Shenzhen, 518107, China.
Li ZhongScientific Research Center, The Seventh Affiliated Hospital of Sun Yat-sen University, Shenzhen, 518107, China.
Nan WangScientific Research Center, The Seventh Affiliated Hospital of Sun Yat-sen University, Shenzhen, 518107, China.
Baiwei ZhaoState Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China.ORCID 0009-0004-2125-8657
Yannan WangSchool of Medicine, Shenzhen Campus of Sun Yat-sen University, Sun Yat-sen University, Shenzhen, 518107, China.
Xinxiang WuScientific Research Center, The Seventh Affiliated Hospital of Sun Yat-sen University, Shenzhen, 518107, China.
Changyu ZhengSchool of Medicine, Shenzhen Campus of Sun Yat-sen University, Sun Yat-sen University, Shenzhen, 518107, China.
Yueheng RuanSchool of Medicine, Shenzhen Campus of Sun Yat-sen University, Sun Yat-sen University, Shenzhen, 518107, China.
Jianfeng HouDepartment of Joint and Trauma Surgery, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510630, China.
Yusheng LuoScientific Research Center, The Seventh Affiliated Hospital of Sun Yat-sen University, Shenzhen, 518107, China.
Yuehan YinScientific Research Center, The Seventh Affiliated Hospital of Sun Yat-sen University, Shenzhen, 518107, China.
Yulong HeDigestive Diseases Center, Guangdong Provincial Key Laboratory of Digestive Cancer Research, The Seventh Affiliated Hospital of Sun Yat-sen University, Shenzhen, 518107, China.ORCID 0000-0002-1902-0963
Andy Peng XiangCenter for Stem Cell Biology and Tissue Engineering, Key Laboratory for Stem Cells and Tissue Engineering, Ministry of Education, Sun Yat-sen University, Guangzhou, 510080, China.ORCID 0000-0003-3409-5012
Jiancheng WangScientific Research Center, The Seventh Affiliated Hospital of Sun Yat-sen University, Shenzhen, 518107, China.ORCID 0000-0001-9599-0171

Funding

Fundamental Research Funds for the Central Universities, Sun Yat-sen University 23ykbj003Guangdong Basic and Applied Basic Research Foundation 2023B1515020016Guangdong Key Scientific Research Platform and Projects for the Higher-educational Institution 2021LSYS003Guangdong Provincial Key Laboratory of Digestive Cancer Research 2021B1212040006National Key Research and Development Program of China Stem Cell and Translational Research 2021YFA1100601National Natural Science Foundation of China 32170799National Natural Science Foundation of China 82100016National Natural Science Foundation of China 82220108013Research Start-up Fund of the Seventh Affiliated Hospital,Sun Yat-sen University ZSQYRSSFAR0003Shenzhen Key Laboratory of Chinese Medicine Active substance screening and Translational Research ZDSYS20220606100801003Shenzhen Medical Research Fund 00201314003
6 · The paper itself

Abstract

Chemotherapy resistance is the main reason of treatment failure in gastric cancer (GC). However, the mechanism of oxaliplatin (OXA) resistance remains unclear. Here, we demonstrate that extracellular mechanical signaling plays crucial roles in OXA resistance within GC. We selected OXA-resistant GC patients and analyzed tumor tissues by single-cell sequencing, and found that the mitochondrial content of GC cells increased in a biosynthesis-independent manner. Moreover, we found that the increased mitochondria of GC cells were mainly derived from mesenchymal stromal cells (MSCs), which could repair the mitochondrial function and reduce the levels of mitophagy in GC cells, thus leading to OXA resistance. Furthermore, we investigated the underlying mechanism and found that mitochondrial transfer was mediated by mechanical signals of the extracellular matrix (ECM). After OXA administration, GC cells actively secreted ECM in the tumor microenvironment (TEM), increasing matrix stiffness of the tumor tissues, which promoted mitochondria to transfer from MSCs to GC cells via microvesicles (MVs). Meanwhile, inhibiting the mechanical-related RhoA/ROCK1 pathway could alleviate OXA resistance in GC cells. In summary, these results indicate that matrix stiffness could be used as an indicator to identify chemotherapy resistance, and targeting mechanical-related pathway could effectively alleviate OXA resistance and improve therapeutic efficacy.

Indexed as

Drug Resistance, NeoplasmMesenchymal Stem CellsMitochondriaOxaliplatinStomach NeoplasmsTumor MicroenvironmentAnimalsAntineoplastic AgentsCell Line, TumorExtracellular MatrixHumansMiceAntineoplastic AgentsOxaliplatingastric cancermatrix stiffnessoxaliplatin resistanceRhoA/ROCK1 signaling pathway

Identifiers

PMID39392399
PMCPMC11653701

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.