Evidence map›Paper›PMID 34184087›Full record

ArticleMolecular medicine reports2021

PI3K/AKT phosphorylation activates ERRα by upregulating PGC‑1α and PGC‑1β in gallbladder cancer.

Lei Wang, Mengmeng Yang, Huihan Jin

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.5field-weighted citation impact, top 43% 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

10 citing papers in PubMed, 13 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

3 authors at 2 institutions in 1 country.

Lei WangDepartment of Hepatobiliary Surgery, The Affiliated Wuxi No. 2 People's Hospital of Nanjing Medical University, Wuxi, Jiangsu 214002, P.R. China.
Mengmeng YangDepartment of Malaria Control and Prevention, Jiangsu Provincial Key Laboratory on Parasite and Vector Control Technology (Jiangsu Institute of Parasitic Diseases), Wuxi, Jiangsu 214002, P.R. China.
Huihan JinDepartment of Hepatobiliary Surgery, The Affiliated Wuxi No. 2 People's Hospital of Nanjing Medical University, Wuxi, Jiangsu 214002, P.R. China.
Nanjing Medical University · CNJiangsu Institute of Parasitic Diseases · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The nuclear estrogen‑related receptor‑α (ERRα) is an orphan receptor that has been identified as a transcriptional factor. Peroxisome proliferator‑activated receptor‑γ (PPARγ) coactivator‑1‑α (PGC‑1α) and PPARγ coactivator‑1‑β (PGC‑1β) act as the co‑activators of ERRα. Our previous study reported that activated ERRα promoted the invasion and proliferation of gallbladder cancer cells by promoting PI3K/AKT phosphorylation. Therefore, the aim of the current study was to investigate whether PI3K/AKT phosphorylation could enhance ERRα activity in a positive feedback loop. LY294002 and insulin‑like growth factor I (IGF‑I) were used to inhibit and promote PI3K/AKT phosphorylation, respectively. A 3X ERE‑TATA luciferase reporter was used to measure ERRα activity. The present study found that LY294002 inhibited PI3K/AKT phosphorylation, decreased the proliferation and invasion of NOZ cells and suppressed the activity of ERRα. Conversely, IGF‑I induced PI3K/AKT phosphorylation, promoted the proliferation and invasion of NOZ cells and enhanced the activity of ERRα. The protein expression levels of PGC‑1α and PGC‑1β were elevated and reduced by IGF‑I and LY294002, respectively. Moreover, knockdown of PGC‑1α and PGC‑1β antagonized ERRα activation, which was enhanced by PI3K/AKT phosphorylation. Taken together, the present study demonstrated that PI3K/AKT phosphorylation triggered ERRα by upregulating the expression levels of PGC‑1α and PGC‑1β in NOZ cells.

Indexed as

Cell Line, TumorCell MovementCell ProliferationChromonesEnzyme InhibitorsERRalpha Estrogen-Related ReceptorGallbladder NeoplasmsGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansInhibitory Concentration 50Insulin-Like Growth Factor IMorpholinesPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPhosphatidylinositol 3-KinasesPhosphorylation2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneChromonesEnzyme InhibitorsERRalpha Estrogen-Related ReceptorInsulin-Like Growth Factor IMorpholinesPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPhosphatidylinositol 3-KinasesPPARGC1A protein, humanPPARGC1B protein, humanProto-Oncogene Proteins c-aktReceptors, EstrogenRNA-Binding Proteinsestrogen‑related receptor‑αgallbladder cancerperoxisome proliferator‑activated receptor‑γ coactivator‑1‑αperoxisome proliferator‑activated receptor‑γ coactivator‑1‑βPI3K/AKT phosphorylation

Identifiers

PMID34184087
PMCPMC8258462
OpenAlexW3173817102

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.