Evidence map›Paper›PMID 30887254›Full record

ArticleInvestigational new drugs2020

The exosome secretion inhibitor neticonazole suppresses intestinal dysbacteriosis-induced tumorigenesis of colorectal cancer.

Lei Gu, Yidong Xu, Wangyan Xu, Meng Li, Hui Su, Cong Li, Zhongchen Liu

Abstract read
PubMed Publisher
In one paragraph

Article in Investigational new drugs, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

12 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. The Emerging Role of Exosomes in Cancer Chemoresistance.Frontiers in cell and developmental biology · 2021
    Review
  9. Review
  10. Review
  11. Review
  12. Article
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.

Lei GuDepartment of General Surgery, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, No. 301 Middle Yanchang Road, Shanghai, 200072, China.
Yidong XuDepartment of General Surgery, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, No. 301 Middle Yanchang Road, Shanghai, 200072, China.
Wangyan XuAnhui University of Science and Technology, Huainan, 232001, Anhui, China.
Meng LiSchool of Medicine Tongji University, Shanghai, 200092, China.
Hui SuAnhui University of Science and Technology, Huainan, 232001, Anhui, China.
Cong LiDepartment of General Surgery, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, No. 301 Middle Yanchang Road, Shanghai, 200072, China.
Zhongchen LiuDepartment of General Surgery, Shanghai Tenth People's Hospital, School of Medicine, Tongji University, No. 301 Middle Yanchang Road, Shanghai, 200072, China. liuzhongchen_10th@163.com.
Tongji University · CNAnhui University of Science and Technology · CNShanghai Tenth People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colorectal cancer (CRC) is the most frequently encountered malignancy associated with the rectum or colon, and accumulating evidences have implicated intestinal dysbacteriosis (IDB, disruption of gut microbiome) and exosomes in the pathology of CRC. We aimed to investigate the effect of IDB on exosome secretion in a CRC xenograft mouse model. An IDB mouse model was established and was inoculated with the CRC cell line SW480 as a xenograft tumor. Tumor growth was monitored for 15 days in sham and IDB mice, after which blood was collected to assess serum exosome secretion. A novel exosome secretion inhibitor, neticonazole, was administered to IDB mice bearing CRC xenograft tumors, followed by monitoring of tumor growth and mouse survival. Western blot analysis was performed in xenograft tumors to investigate the underlying molecular mechanism. IDB promoted CRC xenograft tumor growth and exosome secretion, which could be inhibited by the exosome secretion inhibitor neticonazole. Moreover, neticonazole treatment significantly improved the survival of IDB mice with CRC xenograft tumors, likely through increasing apoptosis of CRC xenograft tumor cells. The exosome secretion inhibitor neticonazole may serve as a promising therapeutic candidate against CRC by suppressing IDB-induced CRC tumorigenesis.

Indexed as

AnimalsAntineoplastic AgentsApoptosisCarcinogenesisCell Line, TumorColorectal NeoplasmsDysbiosisExosomesHumansImidazolesIntestinesMaleMice, Inbred C57BLAntineoplastic AgentsImidazolesneticonazoleColorectal cancerExosomeIntestinal dysbacteriosisNeticonazole

Identifiers

PMID30887254
OpenAlexW2923937013

What OpenQuestion holds

Textmetadata
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.