Evidence map›Paper›PMID 36232604›Full record

ArticleInternational journal of molecular sciences2022

PIKE-A Modulates Mitochondrial Metabolism through Increasing SDHA Expression Mediated by STAT3/FTO Axis.

Mingming Sun, Qi Yan, Yaya Qiao, Huifang Zhao, Yingzhi Wang, Changliang Shan, Shuai Zhang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.8field-weighted citation impact, top 33% 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

3 citing papers in PubMed, 8 citations in OpenAlex.

  1. Abnormal changes in metabolites caused by mJournal of advanced research · 2025
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  2. Review
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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

7 authors at 2 institutions in 1 country.

Mingming SunState Key Laboratory of Medicinal Chemical Biology, College of Pharmacy and Tianjin Key Laboratory of Molecular Drug Research, Nankai University, Tianjin 300350, China.
Qi YanState Key Laboratory of Medicinal Chemical Biology, College of Pharmacy and Tianjin Key Laboratory of Molecular Drug Research, Nankai University, Tianjin 300350, China.
Yaya QiaoState Key Laboratory of Medicinal Chemical Biology, College of Pharmacy and Tianjin Key Laboratory of Molecular Drug Research, Nankai University, Tianjin 300350, China.
Huifang ZhaoSchool of Integrative Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China.
Yingzhi WangState Key Laboratory of Medicinal Chemical Biology, College of Pharmacy and Tianjin Key Laboratory of Molecular Drug Research, Nankai University, Tianjin 300350, China.
Changliang ShanState Key Laboratory of Medicinal Chemical Biology, College of Pharmacy and Tianjin Key Laboratory of Molecular Drug Research, Nankai University, Tianjin 300350, China.ORCID 0000-0002-4906-1686
Shuai ZhangSchool of Integrative Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China.ORCID 0000-0003-0272-0856
Nankai University · CNTianjin University of Traditional Chinese Medicine · CN

Funding

National Nature Science Foundation of China 81902826, 81973356, and 81672781NaturalScience Foundation of Tianjin 21JCZDJC00060the Fundamental Research Funds for the Central Universities of Nankai University 3206054, 91923101, 63213082, and 92122017
6 · The paper itself

Abstract

Previous studies have shown that phosphoinositide 3-kinase enhancer-activating Akt (PIKE-A) is involved in the regulation of several biological processes in cancer. In our previous study, we demonstrated a crucial function of PIKE-A in cancer energy metabolism by regulating pentose phosphate pathway (PPP) flux. However, whether PIKE-A regulates energy metabolism through affecting mitochondrial changes are poorly understood. In the present study, we show that PIKE-A promotes mitochondrial membrane potential, leading to increasing proliferation of glioblastoma cell. Mechanistically, PIKE-A affects the expression of respiratory chain complex Ⅱ succinate dehydrogenase A (SDHA), mediated by regulating the axis of STAT3/FTO. Taken together, these results revealed that inhibition of PIKE-A reduced STAT3/FTO/SDHA expression, leading to the suppression of mitochondrial function. Thus, our findings suggest the PIKE-A/STAT3/FTO/SDHA axis as promising anti-cancer treatment targets.

Indexed as

GlioblastomaProto-Oncogene Proteins c-aktAlpha-Ketoglutarate-Dependent Dioxygenase FTOElectron Transport Complex IIHumansMitochondriaPhosphatidylinositol 3-KinasePhosphatidylinositol 3-KinasesSTAT3 Transcription FactorSuccinate DehydrogenaseAlpha-Ketoglutarate-Dependent Dioxygenase FTOElectron Transport Complex IIFTO protein, humanPhosphatidylinositol 3-KinasePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSDHA protein, humanSTAT3 protein, humanSTAT3 Transcription FactorSuccinate Dehydrogenasecell proliferationglioblastomamitochondriaPIKE-ASDHA

Identifiers

PMID36232604
PMCPMC9570435
OpenAlexW4297235536

What OpenQuestion holds

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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.