Evidence map›Paper›PMID 31988456›Full record

ArticleOncogene2020

Overexpression of PSAT1 promotes metastasis of lung adenocarcinoma by suppressing the IRF1-IFNγ axis.

Yung-Chieh Chan, Yu-Chan Chang, Hsiang-Hao Chuang, Yi-Chieh Yang, Yuan-Feng Lin, Ming-Shyan Huang, Michael Hsiao, Chih-Jen Yang, Kuo-Tai Hua

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
4.3field-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

34 citing papers in PubMed, 58 citations in OpenAlex.

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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

9 authors at 7 institutions in 1 country.

Yung-Chieh Chan *Innovation Center, Show Chwan Memorial Hospital, Changhua, Taiwan.
Yu-Chan Chang *Genomics Research Center, Academia Sinica, Taipei, Taiwan.ORCID http://orcid.org/0000-0003-0474-9935
Hsiang-Hao Chuang *Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan.
Yi-Chieh YangDepartment of Medical Research, Tungs' Taichung MetroHarbor Hospital, Taichung, Taiwan.
Yuan-Feng LinGraduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Ming-Shyan HuangDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, E-DA Cancer Hospital, Kaohsiung, Taiwan.
Michael HsiaoGenomics Research Center, Academia Sinica, Taipei, Taiwan.ORCID http://orcid.org/0000-0001-8529-9213
Chih-Jen YangDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan. chjeya@cc.kmu.edu.tw.
Kuo-Tai HuaGraduate Institute of Toxicology, College of Medicine, National Taiwan University, Taipei, Taiwan. kthua@ntu.edu.tw.
Kaohsiung Medical University · TWChang Bing Show Chwan Memorial Hospital · TWE-Da Hospital · TWGenomics Research Center, Academia Sinica · TWNational Taiwan University · TWTaipei Medical University · TWTungs' Taichung MetroHarbor Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

An increasing number of enzymes involved in serine biosynthesis have been identified and correlated with malignant evolution in various types of cancer. Here we showed that the overexpression of phosphoserine aminotransferase 1 (PSAT1) is widely found in lung cancer tissues compared with nontumor tissues and predicts a poorer prognosis in patients with lung adenocarcinoma. PSAT1 expression was examined in a tissue microarray by immunohistochemistry. The data show that the knockdown of PSAT1 dramatically inhibits the in vitro and in vivo metastatic potential of highly metastatic lung cancer cells; conversely, the enforced expression of exogenous PSAT1 predominantly enhances the metastatic potential of lung cancer cells. Importantly, manipulating PSAT1 expression regulates the in vivo tumor metastatic abilities in lung cancer cells. Adjusting the glucose and glutamine concentrations did not alter the PSAT1-driven cell invasion properties, indicating that this process might not rely on the activation of its enzymatic function. RNA microarray analysis of transcriptional profiling from PSAT1 alternation in CL1-5 and CL1-0 cells demonstrated that interferon regulatory factor 1 (IRF1) acts as a crucial regulator of PSAT1-induced gene expression upon metastatic progression. Decreasing the IRF1-IFIH1 axis compromised the PSAT1-prompted transcriptional reprogramming in cancer cells. Our results identify PSAT1 as a key regulator by a novel PSAT1/IRF1 axis in lung cancer progression, which may serve as a potential biomarker and therapeutic target for the treatment of lung cancer patients.

Indexed as

Adenocarcinoma of LungAnimalsCohort StudiesDisease ProgressionGene Knockdown TechniquesHumansInterferon-gammaInterferon Regulatory Factor-1Lung NeoplasmsMaleMiceNeoplasm InvasivenessNeoplasm MetastasisRNA, MessengerRNA, NeoplasmSignal TransductionIFNG protein, humanInterferon-gammaInterferon Regulatory Factor-1IRF1 protein, humanphosphoserine aminotransferaseRNA, MessengerRNA, NeoplasmTransaminases

Identifiers

PMID31988456
OpenAlexW3003952660

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.