Evidence map›Paper›PMID 35522909›Full record

ArticleClinical and translational medicine2022

Exosome-transmitted miR-769-5p confers cisplatin resistance and progression in gastric cancer by targeting CASP9 and promoting the ubiquitination degradation of p53.

Xinming Jing, Mengyan Xie, Kun Ding, Tingting Xu, Yuan Fang, Pei Ma, Yongqian Shu

Open access · goldAbstract read
In one paragraph

Article in Clinical and translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 3 pooled it
4.9field-weighted citation impact, top 4% 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

39 citing papers in PubMed, 3 syntheses or guidelines pooled it, 60 citations in OpenAlex.

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  4. Mechanisms of chemoresistance in gastric cancer: interplay between microRNAs and the tumor microenvironment.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 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

7 authors at 3 institutions in 1 country.

Xinming JingDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Mengyan XieDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Kun DingDepartment of Molecular Cell Biology & Toxicology, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, China.
Tingting XuDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Yuan FangDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Pei MaDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Yongqian ShuDepartment of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.ORCID 0000-0002-6683-4249
China XD Group (China) · CNJiangsu Province Hospital · CNJiangsu Cancer Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCisplatin resistance is the main cause of poor clinical prognosis in patients with gastric cancer (GC). Yet, the exact mechanism underlying cisplatin resistance remains unclear. Recent studies have suggested that exocrine miRNAs found in the tumor microenvironment participate in tumor metastasis and drug resistance.

methodsExosomes isolated from BGC823 and BGC823/DDP culture medium were characterized by transmission electron microscopy and differential ultracentrifugation, and miRNA expression profiles of BGC823 and BGC823/DDP cells derived exosomes were analyzed using miRNA microarray. In vivo and in vitro assays were used to identify roles of exosomal miR-769-5p and clarify the mechanism of exosomal miR-769-5p regulated the crosstalk between sensitive and resistant GC cells.

resultsIn this study, we found that cisplatin-resistant GC cells communicated with the tumor microenvironment by secreting microvesicles. MiR-769-5p was upregulated in GC tissues and enriched in the serum exosomes of cisplatin-resistant patients. The biologically active miR-769-5p could be integrated into exosomes and delivered to sensitive cells, spreading cisplatin resistance. Underlying cellular and molecular mechanism was miR-769-5p targeting CASP9, thus inhibiting the downstream caspase pathway and promoting the degradation of the apoptosis-related protein p53 through the ubiquitin-proteasome pathway. Targeting miR-769-5p with its antagonist to treat cisplatin-resistant GC cells can restore the cisplatin response, confirming that exosomal miR-769-5p can act as a key regulator of cisplatin resistance in GC.

conclusionsThese findings indicate that exosome-transmitted miR-769-5p confers cisplatin resistance and progression in gastric cancer by targeting CASP9 and promoting the ubiquitination degradation of p53. These findings reveal exosomal miR-769-5p derived from drug-resistant cells can be used as a potential therapeutic predictor of anti-tumor chemotherapy to enhance the effect of anti-cancer chemotherapy, which provides a new treatment option for GC.

Indexed as

ExosomesMicroRNAsStomach NeoplasmsCaspase 9CisplatinDrug Resistance, NeoplasmHumansTumor MicroenvironmentTumor Suppressor Protein p53UbiquitinationCASP9 protein, humanCaspase 9CisplatinMicroRNAsMIRN769 microRNA, humanTumor Suppressor Protein p53CASP9cisplatin resistancegastric cancermiR-769-5pp53

Identifiers

PMID35522909
PMCPMC9076018
OpenAlexW4229000978

What OpenQuestion holds

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LicenceCC BY
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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.