Evidence map›Paper›PMID 29687367›Full record

ArticleJournal of bioenergetics and biomembranes2018

Atovaquone enhances doxorubicin's efficacy via inhibiting mitochondrial respiration and STAT3 in aggressive thyroid cancer.

Zhuo Lv, Xintong Yan, Liying Lu, Chun Su, Yin He

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of bioenergetics and biomembranes, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

27 citing papers in PubMed, 46 citations in OpenAlex.

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  17. IL-6 enhances CD4 cell motility by sustaining mitochondrial CaProceedings of the National Academy of Sciences of the United States of America · 2021
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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

5 authors at 1 institution in 1 country.

Zhuo LvDepartment of Endocrinology, The Third People's Hospital of Guangxi Zhuang Autonomous Region, Riverside Hospital of Guangxi Zhuang Autonomous Region, Heti Road 85, Qingxiu District, Nanning, 530021, China.
Xintong YanDepartment of Endocrinology, The Third People's Hospital of Guangxi Zhuang Autonomous Region, Riverside Hospital of Guangxi Zhuang Autonomous Region, Heti Road 85, Qingxiu District, Nanning, 530021, China.
Liying LuDepartment of Endocrinology, The Third People's Hospital of Guangxi Zhuang Autonomous Region, Riverside Hospital of Guangxi Zhuang Autonomous Region, Heti Road 85, Qingxiu District, Nanning, 530021, China.
Chun SuDepartment of Endocrinology, The Third People's Hospital of Guangxi Zhuang Autonomous Region, Riverside Hospital of Guangxi Zhuang Autonomous Region, Heti Road 85, Qingxiu District, Nanning, 530021, China.
Yin HeDepartment of Endocrinology, The Third People's Hospital of Guangxi Zhuang Autonomous Region, Riverside Hospital of Guangxi Zhuang Autonomous Region, Heti Road 85, Qingxiu District, Nanning, 530021, China. m18776193420@163.com.
Riverside Hospital of Guangxi Zhuang Autonomous Region · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The clinical management of anaplastic thyroid carcinoma and follicular thyroid carcinoma is challenging and requires an alternative therapeutic strategy. Although atovaquone is an FDA-approved anti-malarial drug, studies has recently demonstrated its anti-cancer activities. In line with these efforts, our study shows that atovaquone is an attractive candidate for thyroid cancer treatment. We show that atovaquone significantly inhibits growth, migration and survival in a concentration-dependent manner in 8505C and FTC113 cells. Mechanistically, atovaquone inhibits mitochondrial complex III activity, leading to mitochondrial respiration inhibition and reduction of ATP production in thyroid cancer cells. The inhibitory effects of atovaquone is reversed in mitochondrial respiration-deficient 8505C ρ0 cells, confirming mitochondrial respiration as the mechanism of atovaquone's action in thyroid cancer. In addition, atovaquone suppresses phosphorylation of STAT3 in thyroid cancer wildype but not ρ0 cells, demonstrating that STAT3 phosphorylation inhibition by atovaquone is a consequence of mitochondrial respiration inhibition. Notably, we further demonstrate that atovaquone significantly augments doxorubicin's inhibitory effects via suppressing mitochondrial respiration and STAT3. Our findings suggest that atovaquone can be repurposed for thyroid cancer treatment. Our work also highlights that targeting mitochondrial respiration may represent potential therapeutic strategy in thyroid cancer.

Indexed as

AtovaquoneCell LineCell Line, TumorCell RespirationCell SurvivalDoxorubicinDrug SynergismHumansMitochondriaPhosphorylationSTAT3 Transcription FactorThyroid NeoplasmsAtovaquoneDoxorubicinSTAT3 protein, humanSTAT3 Transcription FactorAtovaquoneDoxorubicinMitochondrial respirationSTAT3Thyroid cancer

Identifiers

PMID29687367
OpenAlexW2801320051

What OpenQuestion holds

Textmetadata
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.