Evidence map›Paper›PMID 40029556›Full record

ArticleHuman cell2025

Poly(I:C) signaling induces robust CXCL10 production and apoptosis in human esophageal squamous cell carcinoma cells.

Yusuke Sato, Akari Yamaya, Kento Sonoda, Akiyuki Wakita, Yushi Nagaki, Ryohei Sasamori, Yoshihiro Sasaki, Takatoshi Yoneya, Shu Nozaki, Tsukasa Takahashi and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Human cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

13 authors.

Yusuke SatoDepartment of Esophageal Surgery, Akita University Hospital, Akita, 010-8543, Japan. yusuke@doc.med.akita-u.ac.jp.ORCID http://orcid.org/0000-0002-2729-7284
Akari YamayaNebuta Research Institute for Life Sciences, Aomori University, Aomori, 030-0943, Japan.
Kento SonodaNebuta Research Institute for Life Sciences, Aomori University, Aomori, 030-0943, Japan.
Akiyuki WakitaDepartment of Esophageal Surgery, Akita University Hospital, Akita, 010-8543, Japan.
Yushi NagakiDepartment of Esophageal Surgery, Akita University Hospital, Akita, 010-8543, Japan.
Ryohei SasamoriDepartment of Esophageal Surgery, Akita University Hospital, Akita, 010-8543, Japan.
Yoshihiro SasakiDepartment of Esophageal Surgery, Akita University Hospital, Akita, 010-8543, Japan.
Takatoshi YoneyaDepartment of Esophageal Surgery, Akita University Hospital, Akita, 010-8543, Japan.
Shu NozakiDepartment of Esophageal Surgery, Akita University Hospital, Akita, 010-8543, Japan.
Tsukasa TakahashiDepartment of Esophageal Surgery, Akita University Hospital, Akita, 010-8543, Japan.
Misako MatsumotoNebuta Research Institute for Life Sciences, Aomori University, Aomori, 030-0943, Japan.
Tsukasa SeyaNebuta Research Institute for Life Sciences, Aomori University, Aomori, 030-0943, Japan.
Kazuhiro ImaiDepartment of Esophageal Surgery, Akita University Hospital, Akita, 010-8543, Japan.

Funding

AMED-SCARDA Grant 233fa827021SPS KAKENHI Grant 19K09210
6 · The paper itself

Abstract

We previously reported that high tumoral expression of Toll-like receptor 3 (TLR3) and CXCL10, a member of the CXC chemokine family, was an independent positive prognostic factor in patients with advanced thoracic esophageal squamous cell carcinoma (ESCC). However, the direct relationships between TLR3 and CXCL10 in ESCC cells was not fully understood. Here, we analyzed TLR3 mRNA and protein expression in two ESCC lines (TE8 and KYSE180) and one esophageal adenocarcinoma (EAC) line (OE19). We also assessed the effect of the TLR3 agonist poly(I:C) on production of downstream adapter proteins and cytokines, including CXCL10, and further tested its effects on cell viability and caspase 3/7 activity with and without siRNA-induced knockdown of TLR3 and the TICAM-1 or MAVS adapter protein. Both ESCC lines, but not the EAC line, showed high expression of TLR3 mRNA and protein. TICAM-1 and MAVS were also expressed, and their knockdown suppressed responsiveness to poly(I:C) in the ESCC lines. Poly(I:C) induced strong CXCL10 production, resulting in significantly upregulated caspase3/7 activity and downregulated cell proliferation in both ESCC lines but not the EAC line. The effect of poly(I:C) on CXCL10 production was attenuated after transfecting the cells with siRNAs targeting TICAM-1 or MAVS. TLR3 is thus highly expressed in ESCC cells, where it induces strong CXCL10 production and significantly upregulates caspase3/7 activity and downregulates cell proliferation. TLR3 signaling and the resultant downstream CXCL10 production have the potential to serve as useful prognostic markers and therapeutic targets for the treatment of ESCC.

Indexed as

ApoptosisCarcinoma, Squamous CellChemokine CXCL10Esophageal NeoplasmsPoly I-CSignal TransductionAdaptor Proteins, Signal TransducingAdaptor Proteins, Vesicular TransportCaspase 3Caspase 7Cell Line, TumorCell ProliferationEsophageal Squamous Cell CarcinomaGene ExpressionHumansRNA, MessengerAdaptor Proteins, Signal TransducingAdaptor Proteins, Vesicular TransportCaspase 3Caspase 7Chemokine CXCL10CXCL10 protein, humanMAVS protein, humanPoly I-CRNA, MessengerTICAM1 protein, humanTLR3 protein, humanToll-Like Receptor 3CXCL10ESCCEsophageal squamous cell carcinomaRLRTLR3Toll-like receptor

Identifiers

PMID40029556
PMCPMC11876272

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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.