Evidence map›Paper›PMID 32460412›Full record

ArticleMolecular oncology2021

FOXD1-AS1 regulates FOXD1 translation and promotes gastric cancer progression and chemoresistance by activating the PI3K/AKT/mTOR pathway.

Qiong Wu, Jiali Ma, Jue Wei, Wenying Meng, Yugang Wang, Min Shi

Open access · goldAbstract read
In one paragraph

Article in Molecular oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
6.6field-weighted citation impact, top 2% 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

54 citing papers in PubMed, 108 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

6 authors at 1 institution in 1 country.

Qiong WuDepartment of Gastroenterology, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, China.ORCID 0000-0001-7965-5410
Jiali MaDepartment of Gastroenterology, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, China.
Jue WeiDepartment of Gastroenterology, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, China.
Wenying MengDepartment of Gastroenterology, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, China.
Yugang WangDepartment of Gastroenterology, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, China.
Min ShiDepartment of Gastroenterology, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, China.
Shanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gastric cancer (GC) is a common gastrointestinal cancer with a high global mortality. Recent reports have suggested that long noncoding RNA (lncRNA) are implicated in multiple aspects of GC, including pathogenesis, progression, and therapeutic response. Herein, we investigated the function of FOXD1-AS1 in GC progression and chemoresistance. Expression of FOXD1-AS1 was low in normal stomach tissues but was upregulated in GC cell lines. Silencing of FOXD1-AS1 impaired GC cell proliferation and motility in vitro, and repressed tumor growth and metastasis in vivo. Importantly, FOXD1-AS1 upregulation increased the resistance of GC cells to cisplatin. Moreover, we found that FOXD1-AS1 promoted FOXD1 protein translation through the eIF4G-eIF4E-eIF4A translational complex. We also demonstrated that FOXD1-AS1 released eIF4E from phosphorylated 4E-BP1 and thereby strengthened the interaction of eIF4E with eIF4G by activating the PI3K/AKT/mTOR pathway. Activation of the PI3K/AKT/mTOR pathway was due to the post-transcriptional upregulation of PIK3CA, in turn induced by FOXD1-AS1-mediated sequestering of microRNA (miR)-466. Furthermore, we verified that FOXD1-AS1 facilitated GC progression and cisplatin resistance in a FOXD1-dependent manner. In conclusion, FOXD1-AS1 aggravates GC progression and chemoresistance by promoting FOXD1 translation via PIK3CA/PI3K/AKT/mTOR signaling. These findings highlight a novel target for treatment of patients GC, particularly patients with cisplatin resistance.

Indexed as

Protein BiosynthesisAdaptor Proteins, Signal TransducingBase SequenceCell Cycle ProteinsCell Line, TumorCell MovementCell ProliferationCisplatinDisease ProgressionDrug Resistance, NeoplasmForkhead Transcription FactorsGene Expression Regulation, NeoplasticHumansMicroRNAsModels, BiologicalNeoplasm MetastasisAdaptor Proteins, Signal TransducingCell Cycle ProteinsCisplatinEIF4EBP1 protein, humanForkhead Transcription FactorsFOXD1 protein, humanMicroRNAsMIRN466 microRNA, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA, Long NoncodingRNA, MessengerTOR Serine-Threonine KinaseseIF4G-eIF4E-eIF4A translational complexFOXD1FOXD1-AS1gastric cancerPI3K/AKT/mTOR pathway

Identifiers

PMID32460412
PMCPMC7782086
OpenAlexW3031953447

What OpenQuestion holds

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LicenceCC BY
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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.