Evidence map›Paper›PMID 40186402›Full record

ArticleThoracic cancer2025

IFI30 Knockdown Inhibits ESCC Progression by Promoting Apoptosis and Senescence via Activation of JNK and P21/P16 Pathways.

Wenyao Xie, Sisi Wei, Caiting Feng, Yuhui Fu, Zhe Zhang, Suli Dai, Cong Zhang, Lianmei Zhao, Baoen Shan

Erratum issuedAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Thoracic cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors.

Wenyao XieResearch Center, The Fourth Hospital of Hebei Medical University, Shijiazhuang, China.ORCID https://orcid.org/0009-0002-3985-9229
Sisi WeiResearch Center, The Fourth Hospital of Hebei Medical University, Shijiazhuang, China.
Caiting FengDepartment of Thoracic Surgery, Handan First Hospital, Handan, China.
Yuhui FuResearch Center, The Fourth Hospital of Hebei Medical University, Shijiazhuang, China.
Zhe ZhangResearch Center, The Fourth Hospital of Hebei Medical University, Shijiazhuang, China.
Suli DaiResearch Center, The Fourth Hospital of Hebei Medical University, Shijiazhuang, China.
Cong ZhangResearch Center, The Fourth Hospital of Hebei Medical University, Shijiazhuang, China.
Lianmei ZhaoResearch Center, The Fourth Hospital of Hebei Medical University, Shijiazhuang, China.
Baoen ShanResearch Center, The Fourth Hospital of Hebei Medical University, Shijiazhuang, China.

Funding

Natural Science Foundation of China 82374090Natural Science Foundation of China U21A20415
6 · The paper itself

Abstract

backgroundEsophageal squamous cell carcinoma (ESCC) is a prevalent and deadly cancer, making it essential to understand the molecular mechanisms influencing its development and prognosis. The role of interferon-gamma-inducible protein 30 (IFI30) in antigen processing is well-established, but its impact on the progression of ESCC remains unclear. This study aimed to investigate the biological function and potential mechanisms of IFI30 in ESCC progression.

methodsPublic databases, proteomics, and immunohistochemistry (IHC) were employed to analyze IFI30 expression. Cell proliferation, migration, and invasion were evaluated using MTS, colony formation, wound healing, and transwell assays. Nude mouse xenograft models were established to assess the effects of IFI30 knockdown in vivo. Quantitative proteomics was utilized to identify differentially expressed proteins (DEPs) and pathways altered by IFI30 knockdown. Cell apoptosis and senescence were evaluated by flow cytometry, SA-β-gal staining, and reactive oxygen species (ROS) analysis.

resultsIFI30 was highly expressed in ESCC and was correlated with advanced stage and poor prognosis. IFI30 knockdown inhibited ESCC cell proliferation, migration, and invasion in vitro and suppressed tumor growth in vivo. DEPs were mainly enriched in biological pathways related to apoptosis, mitophagy, cellular senescence, and lysosome. Furthermore, IFI30 knockdown in ESCC cells upregulated HRAS expression, increased ROS production, activated the JNK signaling pathway, and elevated the expression of P16 and P21, thereby promoting apoptosis and senescence.

conclusionsThis study suggests that IFI30 may regulate the JNK and P21/P16 pathways, exerting pro-tumorigenic effects in ESCC. IFI30 could serve as a potential novel target for ESCC treatment.

Indexed as

Cyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p21Esophageal NeoplasmsEsophageal Squamous Cell CarcinomaAnimalsApoptosisCell MovementCell ProliferationCellular SenescenceDisease ProgressionFemaleGene Knockdown TechniquesHumansMaleMiceMice, NudeCDKN1A protein, humanCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p21apoptosisESCCIFI30JNK pathwaysenescence

Identifiers

PMID40186402
PMCPMC11971534

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.