Evidence map›Paper›PMID 39636345›Full record

ArticleJournal of cancer research and clinical oncology2024

Suppressing GDF15 enhances the chemotherapeutic effect of 5 FU on MSI-H CRC by regulating the ferroptosis pathway SLC7A11/GSH/GPX4.

Zhi Min Huang Fu, Ming Xiao, Hailun Xie, Shuxian Zhang, Tang Yi, Qingshu Li, Ming Li, Yalan Wang

Abstract read
In one paragraph

Article in Journal of cancer research and clinical oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. 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

8 authors.

Zhi Min Huang FuDepartment of Pathology, Molecular Medicine and Cancer Research Center, Department of Clinical Pathololgy, Laboratory of Pathology Diagnostic Center, Chongqing Medical University, Chongqing, China.
Ming XiaoDepartment of Pathology, Molecular Medicine and Cancer Research Center, Department of Clinical Pathololgy, Laboratory of Pathology Diagnostic Center, Chongqing Medical University, Chongqing, China.
Hailun XieDepartment of Pathology, Molecular Medicine and Cancer Research Center, Department of Clinical Pathololgy, Laboratory of Pathology Diagnostic Center, Chongqing Medical University, Chongqing, China.
Shuxian ZhangDepartment of Pathology, Molecular Medicine and Cancer Research Center, Department of Clinical Pathololgy, Laboratory of Pathology Diagnostic Center, Chongqing Medical University, Chongqing, China.
Tang YiDepartment of Pathology, Molecular Medicine and Cancer Research Center, Department of Clinical Pathololgy, Laboratory of Pathology Diagnostic Center, Chongqing Medical University, Chongqing, China.
Qingshu LiDepartment of Pathology, Molecular Medicine and Cancer Research Center, Department of Clinical Pathololgy, Laboratory of Pathology Diagnostic Center, Chongqing Medical University, Chongqing, China.
Ming LiDepartment of Pathology, Molecular Medicine and Cancer Research Center, Department of Clinical Pathololgy, Laboratory of Pathology Diagnostic Center, Chongqing Medical University, Chongqing, China. 500309@hospital.cqmu.edu.cn.
Yalan WangDepartment of Pathology, Molecular Medicine and Cancer Research Center, Department of Clinical Pathololgy, Laboratory of Pathology Diagnostic Center, Chongqing Medical University, Chongqing, China. wangyalan@cqmu.edu.cn.

Funding

Chongqing Education Committee science and technology research project X4557
6 · The paper itself

Abstract

Growth differentiation factor 15 (GDF15) is a member of the transforming growth factor beta (TGF-β) superfamily and is related to metabolism, injury, and aging. GDF15 has both tumor-promoting and tumor-suppressing effects. However, its role in colorectal cancer (CRC) with high microsatellite instability (MSI-H) must be further clarified. In our study, we found that GDF15 is generally elevated in pancarcinoma, particularly in colorectal cancer, and serves as an early indicator of the development of colorectal cancer. IHC and WB confirmed that GDF15 was elevated in MSI-H CRC clinical tissues and MSI-H CRC cell lines (HCT-116 and LoVo). Suppressing GDF15 by siRNA resulted in a substantial decrease in cell viability and proliferation. Furthermore, suppressing GDF15 can increase the sensitivity of MSI-H CRC cells to 5-fluorouracil (5-FU), which decreases cell viability and increases the apoptosis rate. In vivo experiments also demonstrated that mouse xenografts with suppressed GDF15 expression were more susceptible to 5-FU chemotherapy. We examined alterations in mitochondria via electron microscopy and changes in the mitochondrial membrane potential, ferroptosis-related signals (MDA, Fe

Indexed as

Colorectal NeoplasmsFerroptosisFluorouracilGrowth Differentiation Factor 15AnimalsAntimetabolites, AntineoplasticCell Line, TumorCell ProliferationFemaleHCT116 CellsHumansMaleMiceMice, Inbred BALB CMice, NudeMicrosatellite InstabilityAntimetabolites, AntineoplasticFluorouracilGDF15 protein, humanGrowth Differentiation Factor 15Colorectal cancerFerroptosisGDF15Microsatellite instability high

Identifiers

PMID39636345
PMCPMC11621149

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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.