Evidence map›Paper›PMID 37888748›Full record

ArticleInternational journal of oncology2023

Novel insights into the ecDNA formation mechanism involving MSH3 in methotrexate‑resistant human colorectal cancer cells.

Xu Wang, Yanan Qu, Ruonan Xing, Jing Zhou, Yanghe Liu, Huishu Zhang, Jing Zhu, Jinfa Ma, Xiaobo Cui, Tiantian Song and 6 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

5 citing papers in PubMed, 11 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Review
  5. Review
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

16 authors at 1 institution in 1 country.

Xu Wang *Laboratory of Medical Genetics, Harbin Medical University, Harbin, Heilongjiang 150081, P.R. China.
Yanan Qu *Laboratory of Medical Genetics, Harbin Medical University, Harbin, Heilongjiang 150081, P.R. China.
Ruonan Xing *Laboratory of Medical Genetics, Harbin Medical University, Harbin, Heilongjiang 150081, P.R. China.
Jing ZhouLaboratory of Medical Genetics, Harbin Medical University, Harbin, Heilongjiang 150081, P.R. China.
Yanghe LiuLaboratory of Medical Genetics, Harbin Medical University, Harbin, Heilongjiang 150081, P.R. China.
Huishu ZhangLaboratory of Medical Genetics, Harbin Medical University, Harbin, Heilongjiang 150081, P.R. China.
Jing ZhuLaboratory of Medical Genetics, Harbin Medical University, Harbin, Heilongjiang 150081, P.R. China.
Jinfa MaLaboratory of Medical Genetics, Harbin Medical University, Harbin, Heilongjiang 150081, P.R. China.
Xiaobo CuiLaboratory of Medical Genetics, Harbin Medical University, Harbin, Heilongjiang 150081, P.R. China.
Tiantian SongLaboratory of Medical Genetics, Harbin Medical University, Harbin, Heilongjiang 150081, P.R. China.
Shukai XingLaboratory of Medical Genetics, Harbin Medical University, Harbin, Heilongjiang 150081, P.R. China.
Guohua JiLaboratory of Medical Genetics, Harbin Medical University, Harbin, Heilongjiang 150081, P.R. China.
Peng LiuLaboratory of Medical Genetics, Harbin Medical University, Harbin, Heilongjiang 150081, P.R. China.
Wenjing SunLaboratory of Medical Genetics, Harbin Medical University, Harbin, Heilongjiang 150081, P.R. China.
Songbin FuLaboratory of Medical Genetics, Harbin Medical University, Harbin, Heilongjiang 150081, P.R. China.
Xiangning MengLaboratory of Medical Genetics, Harbin Medical University, Harbin, Heilongjiang 150081, P.R. China.
Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Extrachromosomal DNAs (ecDNAs), also known as double minutes (DMs), can induce a fast increase in gene copy numbers and promote the development of cancer, including drug resistance. MutS homolog 3 (MSH3), a key protein in mismatch repair, has been indicated to participate in the regulation of DNA double‑strand break (DSB) repair, which has been reported to be associated with the formation of ecDNAs. However, it remains unclear whether MSH3 can influence drug resistance via ecDNAs in cancer. In the present study, high MSH3 expression was observed in methotrexate (MTX)‑resistant HT29 cells [DM‑ and homogeneously staining region (HSR)‑containing cells] compared with parental HT29 cells. Additionally, decreased amounts of ecDNAs, HSRs and amplified genes locating on ecDNAs and HSRs were detected following depletion of MSH3 and this could be reversed by overexpressing MSH3 in DM‑containing cells. No corresponding changes were found in HSR‑containing cells. The present study further verified the involvement of MSH3‑regulated DNA DSB repair pathways in the formation of ecDNAs by detecting the expression of core proteins and pathway activity. Furthermore, expulsion of ecDNAs/HSRs was detected and increased frequencies of micronuclei/nuclear buds with dihydrofolate reductase (

Indexed as

Colorectal NeoplasmsMethotrexateChromosome AberrationsDNADNA-Binding ProteinsDNA RepairHumansMutS Homolog 3 ProteinDNADNA-Binding ProteinsMethotrexateMSH3 protein, humanMutS Homolog 3 ProteincancerDNA double‑strand breaksextrachromosomal DNAsmethotrexate‑resistanceMutS homolog 3

Identifiers

PMID37888748
PMCPMC10631765
OpenAlexW4387814471

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.