Evidence map›Paper›PMID 33152171›Full record

ArticleMolecular oncology2021

Multi-kinase framework promotes proliferation and invasion of lung adenocarcinoma through activation of dynamin-related protein 1.

Kuei-Pin Chung, Yen-Lin Huang, Yi-Jung Chen, Yi-Hsiu Juan, Chia-Lang Hsu, Kiichi Nakahira, Yen-Tsung Huang, Mong-Wei Lin, Shang-Gin Wu, Jin-Yuan Shih and 2 more

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 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

13 citing papers in PubMed, 16 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

12 authors at 3 institutions in 2 countries.

Kuei-Pin ChungDepartment of Laboratory Medicine, National Taiwan University Hospital and National Taiwan University Cancer Center, Taipei, Taiwan.ORCID 0000-0003-1916-8068
Yen-Lin HuangDepartment of Pathology, National Taiwan University Hospital and National Taiwan University Cancer Center, Taipei, Taiwan.
Yi-Jung ChenDepartment of Laboratory Medicine, National Taiwan University Hospital and National Taiwan University Cancer Center, Taipei, Taiwan.
Yi-Hsiu JuanDepartment of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan.
Chia-Lang HsuDepartment of Medical Research, National Taiwan University Hospital, Taipei, Taiwan.
Kiichi NakahiraDepartment of Pharmacology, Nara Medical University, Kashihara, Nara, Japan.
Yen-Tsung HuangInstitute of Statistical Science, Academia Sinica, Taipei, Taiwan.
Mong-Wei LinDepartment of Surgery, National Taiwan University Hospital, Taipei, Taiwan.
Shang-Gin WuDepartment of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan.
Jin-Yuan ShihDepartment of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan.
Yih-Leong ChangDepartment of Pathology, National Taiwan University Hospital and National Taiwan University Cancer Center, Taipei, Taiwan.
Chong-Jen YuDepartment of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan.
National Taiwan University Hospital · TWNational Taiwan University · TWNara Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies revealed the role of dynamin-related protein 1 (DRP1), encoded by the DNM1L gene, in regulating the growth of cancer cells of various origins. However, the regulation, function, and clinical significance of DRP1 remain undetermined in lung adenocarcinoma. Our study shows that the expression and activation of DRP1 are significantly correlated with proliferation and disease extent, as well as an increased risk of postoperative recurrence in stage I to stage IIIA lung adenocarcinoma. Loss of DRP1 in lung adenocarcinoma cell lines leads to an altered mitochondrial morphology, fewer copies of mitochondrial DNA, decreased respiratory complexes, and impaired oxidative phosphorylation. Additionally, the proliferation and invasion are both suppressed in DRP1-depleted lung adenocarcinoma cell lines. Our data further revealed that DRP1 activation through serine 616 phosphorylation is regulated by ERK/AKT and CDK2 in lung adenocarcinoma cell lines. Collectively, we propose the multikinase framework in activating DRP1 in lung adenocarcinoma to promote the malignant properties. Biomarkers related to mitochondrial reprogramming, such as DRP1, can be used to evaluate the risk of postoperative recurrence in early-stage lung adenocarcinoma.

Indexed as

Cell ProliferationAdenocarcinoma of LungAnimalsCell Line, TumorDynaminsFemaleHumansLung NeoplasmsMaleMiceMice, KnockoutMice, NudeNeoplasm InvasivenessNeoplasm ProteinsProtein KinasesDNM1L protein, humanDynaminsNeoplasm ProteinsProtein Kinasescyclin-dependent kinase 2dynamin-related protein 1glycolytic serine synthesislung adenocarcinomamitochondriaprognosis

Identifiers

PMID33152171
PMCPMC7858280
OpenAlexW3094793504

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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.