Evidence map›Paper›PMID 38433313›Full record

ArticleCancer science2024

Mitochondrial fission enhances IL-6-induced metastatic potential in ovarian cancer via ERK1/2 activation.

Juwon Lee, Youngjin Han, Soochi Kim, HyunA Jo, Wenyu Wang, Untack Cho, Se Ik Kim, Boyun Kim, Yong Sang Song

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

Article in Cancer science, 2024. 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
2.3field-weighted citation impact, top 12% 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, 10 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

9 authors at 4 institutions in 4 countries.

Juwon LeeWCU Biomodulation, Department of Agricultural Biotechnology, Seoul National University, Seoul, Korea.
Youngjin HanCancer Research Institute, College of Medicine, Seoul National University, Seoul, Korea.
Soochi KimDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California, USA.
HyunA JoWCU Biomodulation, Department of Agricultural Biotechnology, Seoul National University, Seoul, Korea.
Wenyu WangDepartment of Medical Oncology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China.
Untack ChoCancer Research Institute, College of Medicine, Seoul National University, Seoul, Korea.
Se Ik KimDepartment of Obstetrics and Gynecology, College of Medicine, Seoul National University, Seoul, Korea.
Boyun KimDepartment of SmartBio, College of Life and Health Science, Kyungsung University, Busan, Korea.
Yong Sang SongWCU Biomodulation, Department of Agricultural Biotechnology, Seoul National University, Seoul, Korea.ORCID https://orcid.org/0000-0001-7115-4021
Seoul National University · KRKyungsung University · KRStanford University · USZhejiang Chinese Medical University · CN

Funding

2022 cancer research support project CB-2022-A-2Korea Health Technology R&D Project HI16C2037
6 · The paper itself

Abstract

Ovarian cancer is a lethal gynecologic cancer mostly diagnosed in an advanced stage with an accumulation of ascites. Interleukin-6 (IL-6), a pro-inflammatory cytokine is highly elevated in malignant ascites and plays a pleiotropic role in cancer progression. Mitochondria are dynamic organelles that undergo fission and fusion in response to external stimuli and dysregulation in their dynamics has been implicated in cancer progression and metastasis. Here, we investigate the effect of IL-6 on mitochondrial dynamics in ovarian cancer cells (OVCs) and its impact on metastatic potential. Treatment with IL-6 on ovarian cancer cell lines (SKOV3 and PA-1) led to an elevation in the metastatic potential of OVCs. Interestingly, a positive association was observed between dynamin-related protein 1 (Drp1), a regulator of mitochondrial fission, and IL-6R in metastatic ovarian cancer tissues. Additionally, IL-6 treatment on OVCs was linked to the activation of Drp1, with a notable increase in the ratio of the inhibitory form p-Drp1(S637) to the active form p-Drp1(S616), indicating enhanced mitochondrial fission. Moreover, IL-6 treatment triggered the activation of ERK1/2, and inhibiting ERK1/2 mitigated IL-6-induced mitochondrial fission. Suppressing mitochondrial fission through siRNA transfection and a pharmacological inhibitor reduced the IL-6-induced migration and invasion of OVCs. This was further supported by 3D invasion assays using patient-derived spheroids. Altogether, our study suggests the role of mitochondrial fission in the metastatic potential of OVCs induced by IL-6. The inhibition of mitochondrial fission could be a potential therapeutic approach to suppress the metastasis of ovarian cancer.

Indexed as

DynaminsInterleukin-6MAP Kinase Signaling SystemMitochondrial DynamicsOvarian NeoplasmsCell Line, TumorCell MovementFemaleHumansMitochondriaNeoplasm MetastasisReceptors, Interleukin-6DynaminsInterleukin-6Receptors, Interleukin-6Drp13IL‐62metastasis5mitochondria1ovarian cancer4

Identifiers

PMID38433313
PMCPMC11093201
OpenAlexW4392401729

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.