Evidence map›Paper›PMID 36293209›Full record

ArticleInternational journal of molecular sciences2022

Modulating p-AMPK/mTOR Pathway of Mitochondrial Dysfunction Caused by MTERF1 Abnormal Expression in Colorectal Cancer Cells.

Qianqian Liu, Longlong Zhang, Yayan Zou, Ying Tao, Bing Wang, Bin Li, Ruai Liu, Boyong Wang, Lei Ding, Qinghua Cui and 4 more

Open access · goldAbstract read
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 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

9 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
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  4. Review
  5. Article
  6. Mitochondria transcription and cancer.Cell death discovery · 2024
    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

14 authors at 3 institutions in 1 country.

Qianqian LiuSchool of Life Sciences, Yunnan University, Kunming 650091, China.
Longlong ZhangSchool of Life Sciences, Yunnan University, Kunming 650091, China.
Yayan ZouSchool of Life Sciences, Yunnan University, Kunming 650091, China.
Ying TaoSchool of Life Sciences, Yunnan University, Kunming 650091, China.
Bing WangSchool of Life Sciences, Yunnan University, Kunming 650091, China.
Bin LiCollege of Basic Medical Sciences, Dali University, Dali 671000, China.
Ruai LiuCollege of Basic Medical Sciences, Dali University, Dali 671000, China.
Boyong WangCollege of Basic Medical Sciences, Dali University, Dali 671000, China.
Lei DingSchool of Life Sciences, Yunnan University, Kunming 650091, China.
Qinghua CuiSchool of Life Sciences, Yunnan University, Kunming 650091, China.
Jie LinSchool of Life Sciences, Yunnan University, Kunming 650091, China.
Bingyu MaoState Key Laboratory of Genetic Resources and Evolution, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming 650223, China.
Wei XiongCollege of Basic Medical Sciences, Dali University, Dali 671000, China.
Min YuSchool of Life Sciences, Yunnan University, Kunming 650091, China.
Yunnan University · CNDali University · CNChinese Academy of Sciences · CN

Funding

d Yunnan University's Research In-novation Fund for Graduate Students 2020267, 2021Y314National Nature Science Foundation of China 32160167, 31760331, 31260276, 31601155, 81860531, 81760507, 82160516the Applied Basic Research Programs of Science and Technology Department of Yunnan Province 202101AT070006the Key Project of Science and Technology Department of Yunnan Province 202001BB0500080, 202001BB050041the Reserve Talents of Young and Middle-aged Academic and Technical Leaders of Yunnan Province No. 2017HB077
6 · The paper itself

Abstract

Human mitochondrial transcription termination factor 1 (MTERF1) has been demonstrated to play an important role in mitochondrial gene expression regulation. However, the molecular mechanism of MTERF1 in colorectal cancer (CRC) remains largely unknown. Here, we found that MTERF1 expression was significantly increased in colon cancer tissues compared with normal colorectal tissue by Western blotting, immunohistochemistry, and tissue microarrays (TMA). Overexpression of MTERF1 in the HT29 cell promoted cell proliferation, migration, invasion, and xenograft tumor formation, whereas knockdown of MTERF1 in HCT116 cells appeared to be the opposite phenotype to HT29 cells. Furthermore, MTERF1 can increase mitochondrial DNA (mtDNA) replication, transcription, and protein synthesis in colorectal cancer cells; increase ATP levels, the mitochondrial crista density, mitochondrial membrane potential, and oxygen consumption rate (OCR); and reduce the ROS production in colorectal cancer cells, thereby enhancing mitochondrial oxidative phosphorylation (OXPHOS) activity. Mechanistically, we revealed that MTERF1 regulates the AMPK/mTOR signaling pathway in cancerous cell lines, and we also confirmed the involvement of the AMPK/mTOR signaling pathway in both xenograft tumor tissues and colorectal cancer tissues. In summary, our data reveal an oncogenic role of MTERF1 in CRC progression, indicating that MTERF1 may represent a new therapeutic target in the future.

Indexed as

Colonic NeoplasmsColorectal NeoplasmsAdenosine TriphosphateAMP-Activated Protein KinasesCell Line, TumorCell ProliferationDNA, MitochondrialGene Expression Regulation, NeoplasticHCT116 CellsHumansMitochondriaReactive Oxygen SpeciesTOR Serine-Threonine KinasesAdenosine TriphosphateAMP-Activated Protein KinasesDNA, MitochondrialMTOR protein, humanReactive Oxygen SpeciesTOR Serine-Threonine KinasesAMPK/mTORcell proliferationcolorectal cancermtDNAMTERF1oxidative phosphorylation

Identifiers

PMID36293209
PMCPMC9604058
OpenAlexW4306385412

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.