Evidence map›Paper›PMID 37672204›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2024

Overexpressed FAM111B degrades GSDMA to promote esophageal cancer tumorigenesis and cisplatin resistance.

Haiqin Wang, Haohui Wang, Jiajing Chen, Pian Liu, Xiaoxiong Xiao

Abstract read
In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

13 citing papers in PubMed, 14 citations in OpenAlex.

  1. The gasdermin family: from pyroptosis mechanisms to therapeutic targets.Signal transduction and targeted therapy · 2026
    Review
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  3. Article
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  9. Role of gasdermins in chronic kidney disease.Frontiers in immunology · 2025
    Review
  10. Review
  11. Review
  12. Identification of Tumor SuppressiveInternational journal of molecular sciences · 2024
    Article
  13. The gasdermin family: emerging therapeutic targets in diseases.Signal transduction and targeted therapy · 2024
    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

5 authors at 3 institutions in 1 country.

Haiqin WangDepartment of Geriatrics, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Haohui WangDepartment of Thoracic Surgery, The Second Xiangya Hospital of Central South University, Changsha, Hunan, China.
Jiajing ChenDepartment of Geriatrics, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Pian LiuUnion Hospital, Tongji Medical College, Huazhong University of Science and Technology, Cancer Center, Wuhan, Hubei, China. liupian@hust.edu.cn.
Xiaoxiong XiaoDepartment of Thoracic Surgery, Xiangya Hospital, Central South University, Changsha, Hunan, China. xiaoxx1988@csu.edu.cn.
Central South University · CNHuazhong University of Science and Technology · CNSecond Xiangya Hospital of Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChemotherapeutic agents such as cisplatin are commonly used in patients with clinically unresectable or recurrent esophageal cancer (ESCA). However, patients often develop resistance to cisplatin, which in turn leads to a poor prognosis. Studies have shown that FAM111B may be involved in the development of tumors as an oncogene or tumor suppressor gene. However, the pathological role and corresponding mechanism of FAM111B in ESCA are still unclear.

methodsThe GEPIA web tool, ENCORI Pan-Cancer Analysis Platform and UALCAN-TCGA database were used to study the expression of FAM111B in ESCA. CCK-8, angiogenesis, Transwell and xenograft assays were applied to explore the biological function of FAM111B in ESCA. Western blot, RT-qPCR, and RNA-seq analyses were applied to study the FAM111B/GSDMA axis in the progression of ESCA cells. CCK-8 and xenograft assays were used to study the role of the FAM111B/GSDMA axis in determining the sensitivity of ESCA to cisplatin.

resultsOur results demonstrated that FAM111B is highly expressed in ESCA tissues compared to normal tissues. We showed that FAM111B promotes the progression of ESCC cells by binding to GSDMA and that the trypsin protease domain is essential for the activity of FAM111B. Furthermore, we showed that the FAM111B/GSDMA axis regulates cisplatin sensitivity in ESCA.

conclusionsOverall, we identified a novel FAM111B/GSDMA axis regulating ESCA tumorigenesis and chemosensitivity, at least in ESCC cells.

Indexed as

Cell Cycle ProteinsCisplatinEsophageal NeoplasmsGasderminsCarcinogenesisCell Transformation, NeoplasticDrug Resistance, NeoplasmHumansSincalideCell Cycle ProteinsCisplatinFAM111B protein, humanGasderminsGSDMA protein, humanSincalideCisplatinEsophageal cancerFAM111BGSDMA

Identifiers

PMID37672204
PMCPMC12974030
OpenAlexW4386467226

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.