Evidence map›Paper›PMID 35858011›Full record

ArticleClinical and translational medicine2022

S100A14: A novel negative regulator of cancer stemness and immune evasion by inhibiting STAT3-mediated programmed death-ligand 1 expression in colorectal cancer.

Hye-Young Min, Jaebeom Cho, Jeong Yeon Sim, Hye-Jin Boo, Ji-Sun Lee, Seon-Boon Lee, Young-Jin Lee, Sung Joo Kim, Kyu-Pyo Kim, In-Ja Park and 5 more

Open access · goldAbstract read
In one paragraph

Article in Clinical and translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

14 citing papers in PubMed, 18 citations in OpenAlex.

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  6. Regulation of Cancer Stem Cells in the Tumor Microenvironment.Cancer heterogeneity and plasticity · 2025
    Article
  7. Breaking Immunosuppression to Enhance Cancer Stem Cell-Targeted Immunotherapy.International journal of biological sciences · 2025
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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

15 authors at 4 institutions in 4 countries.

Hye-Young MinCreative Research Initiative Center for Concurrent Control of Emphysema and Lung Cancer, College of Pharmacy, Seoul National University, Seoul, Republic of Korea.
Jaebeom ChoCreative Research Initiative Center for Concurrent Control of Emphysema and Lung Cancer, College of Pharmacy, Seoul National University, Seoul, Republic of Korea.
Jeong Yeon SimCreative Research Initiative Center for Concurrent Control of Emphysema and Lung Cancer, College of Pharmacy, Seoul National University, Seoul, Republic of Korea.
Hye-Jin BooCreative Research Initiative Center for Concurrent Control of Emphysema and Lung Cancer, College of Pharmacy, Seoul National University, Seoul, Republic of Korea.
Ji-Sun LeeCreative Research Initiative Center for Concurrent Control of Emphysema and Lung Cancer, College of Pharmacy, Seoul National University, Seoul, Republic of Korea.
Seon-Boon LeeDepartment of Biochemistry and Cell Biology, School of Medicine, Cell & Matrix Research Institute, Kyungpook National University, Daegu, Republic of Korea.
Young-Jin LeeDepartment of Biochemistry and Cell Biology, School of Medicine, Cell & Matrix Research Institute, Kyungpook National University, Daegu, Republic of Korea.
Sung Joo KimDepartment of Pathology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea.
Kyu-Pyo KimDepartment of Oncology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea.
In-Ja ParkDepartment of Surgery, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea.
Seung-Mo HongDepartment of Pathology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea.
Xue-Li ZhangState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, P.R. China.
Zhi-Gang ZhangState Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, P.R. China.ORCID 0000-0001-8965-223X
Rang-Woon ParkDepartment of Biochemistry and Cell Biology, School of Medicine, Cell & Matrix Research Institute, Kyungpook National University, Daegu, Republic of Korea.
Ho-Young LeeCreative Research Initiative Center for Concurrent Control of Emphysema and Lung Cancer, College of Pharmacy, Seoul National University, Seoul, Republic of Korea.ORCID 0000-0001-7556-9312
Seoul National University · KRUlsan College · KRKyungpook National University · KRShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundProgrammed death-ligand 1 (PD-L1) has functional roles in cancer stem-like cell (CSC) phenotypes and chemoresistance besides immune evasion. Chemotherapy is a common treatment choice for colorectal cancer (CRC) patients; however, chemoresistance limits its effectiveness of treatment.

methodsWe examined the role of S100A14 (SA14) in CRC by adopting PD-L1

resultsWe identified a novel function of SA14 as a regulator of immune surveillance, major CSC phenotypes, and survival capacity under hostile microenvironments, including those harbouring chemotherapeutics, and as a prognostic biomarker in CRC. Mechanistically, SA14 inhibits PD-L1 expression by directly interacting with signal transducer and activator of transcription 3 (STAT3) and inducing its proteasome-mediated degradation. While gain-of-SA14 causes loss of PD-L1 expression and tumourigenic potential and sensitisation to chemotherapy-induced apoptosis in chemoresistant CRC cells, loss-of-SA14 causes increases in PD-L1 expression, tumourigenic potential, and chemoresistance in vitro and in vivo. We further show that a combinatorial treatment with chemotherapy and recombinant SA14 protein effectively induces apoptosis in PD-L1

conclusionsOur results suggest that SA14-based therapy is an effective strategy to prevent tumour progression and that SA14 is a predictive biomarker for anti-PD-L1 immunotherapy and chemotherapy in combination.

Indexed as

Colorectal NeoplasmsSTAT3 Transcription FactorB7-H1 AntigenCalcium-Binding ProteinsHumansImmune EvasionTumor MicroenvironmentB7-H1 AntigenCalcium-Binding ProteinsCD274 protein, humanS100A14 protein, humanSTAT3 protein, humanSTAT3 Transcription Factorcancer stem-like cellscolorectal cancerPD-L1S100A14STAT3

Identifiers

PMID35858011
PMCPMC9299575
OpenAlexW4286261453

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.