Evidence map›Paper›PMID 39511680›Full record

ArticleBiology direct2024

FXR1 associates with and degrades PDZK1IP1 and ATOH8 mRNAs and promotes esophageal cancer progression.

Faiz Ali Khan, Dalia Fouad, Farid S Ataya, Na Fang, Jingcheng Dong, Shaoping Ji

Abstract read
In one paragraph

Article in Biology direct, 2024. 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
–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

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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.

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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

6 authors.

Faiz Ali KhanDepartment of Integrative Medicine, Huashan Hospital, Fudan University, Middle Urumqi Road, Shanghai, China.
Dalia FouadDepartment of Zoology, College of Science, King Saud University, Riyadh, Saudi Arabia.
Farid S AtayaDepartment of Biochemistry, College of Science, King Saud University, Riyadh, Saudi Arabia.
Na FangLaboratory of Cell Signal Transduction, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Henan University, Kaifeng, Henan, 475004, China. fangna@henu.edu.cn.
Jingcheng DongDepartment of Integrative Medicine, Huashan Hospital, Fudan University, Middle Urumqi Road, Shanghai, China. jcdong2004@126.com.
Shaoping JiLaboratory of Cell Signal Transduction, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Henan University, Kaifeng, Henan, 475004, China. shaopingji@henu.edu.cn.

Funding

National Natural Science Foundation of China No.31371386The Researchers Supporting Project, King Saud University, Riyadh, Saudi Arabia RSPD2024R965
6 · The paper itself

Abstract

backgroundThe growing body of evidence suggests that RNA-binding proteins (RBPs) have an important function in cancer biology. This research characterizes the expression status of fragile X-related protein 1 (FXR1) in esophageal cancer (ESCA) cell lines and understands its mechanistic importance in ESCA tumor biology.

methodsThe role of FXR1, PDZK1IP1, and ATOH8 in the malignant biological behaviors of ESCA cells was investigated using in-vitro and in-vivo experiments.

resultsFXR1 was aberrantly overexpressed at both the transcript and protein levels in ESCA cells. Deficiency of FXR1 in ESCA cells was associated with decreased cell proliferation, viability and compromised cell migration compared to the control group. In addition, the inhibition of FXR1 leads to the promotion of apoptosis and cell cycle arrest in ESCA cells. Furthermore, FXR1 knockdown stabilizes senescence markers, promoting cellular senescence and decreasing cancer growth. Mechanistically, FXR1 negatively regulated PDZK1IP1 or ATOH8 transcripts by promoting mRNA degradation via direct interaction with its 3'UTR. PDZK1IP1 or ATOH8 overexpression predominantly inhibited the tumor-promotive phenotype in FXR1-overexpressed cells. Furthermore, FXR1 inhibition and PDZK1IP1 or ATOH8 overexpression in combination with FXR1-overexpressed cells significantly decreased xenograft tumor formation and enhanced nude mouse survival without causing apparent toxicity (P < 0.01). In the FXR1 knockdown group, the tumor weight of mice decreased by 80% compared to the control group (p < 0.01).

conclusionsOur results demonstrate FXR1's oncogenic involvement in ESCA cell lines, suggesting that FXR1 may be implicated in ESCA development by regulating the stability of PDZK1IP1 and ATOH8 mRNAs. For the first time, our findings emphasize the importance of FXR1-PDZK1IP1 and -ATOH8 functional modules in the development of ESCA, which might have potential diagnostic or therapeutic implications.

Indexed as

Esophageal NeoplasmsRNA-Binding ProteinsRNA, MessengerAnimalsApoptosisBasic Helix-Loop-Helix ProteinsCell Line, TumorCell MovementCell ProliferationDisease ProgressionGene Expression Regulation, NeoplasticHumansMiceMice, NudeBasic Helix-Loop-Helix ProteinsFXR1 protein, humanRNA-Binding ProteinsRNA, MessengerATOH8FXR1MalignancyPDZK1IP1RNA binding proteins

Identifiers

PMID39511680
PMCPMC11542266

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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.