Evidence map›Paper›PMID 31953926›Full record

ArticleCancer medicine2020

Effects of propofol on colon cancer metastasis through STAT3/HOTAIR axis by activating WIF-1 and suppressing Wnt pathway.

Yun-Fei Zhang, Chang-Sheng Li, Yi Zhou, Xi-Hua Lu

Open access · goldAbstract read
In one paragraph

Article in Cancer medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
8.3field-weighted citation impact, top 2% 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

40 citing papers in PubMed, 63 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

4 authors at 1 institution in 1 country.

Yun-Fei ZhangDepartment of Anesthesiology, Affiliated Cancer Hospital of Zhengzhou University, Henan Cancer Hospital, Zhengzhou, P.R. China.
Chang-Sheng LiDepartment of Anesthesiology, Affiliated Cancer Hospital of Zhengzhou University, Henan Cancer Hospital, Zhengzhou, P.R. China.
Yi ZhouDepartment of Anesthesiology, Affiliated Cancer Hospital of Zhengzhou University, Henan Cancer Hospital, Zhengzhou, P.R. China.
Xi-Hua LuDepartment of Anesthesiology, Affiliated Cancer Hospital of Zhengzhou University, Henan Cancer Hospital, Zhengzhou, P.R. China.ORCID 0000-0001-9033-9363
Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIn the present study, we aim to investigate the potential role of propofol in the tumor progression of colon cancer.

methodsHuman colon cancer cell lines were cultured and exposed with 8 μg/mL propofol. RNA interference was performed to silence the expression of HOTAIR or STAT3 to explore their biological functions in colon cancer. Cell apoptosis and invasion were assessed using flow cytometry and transwell assays, respectively. Quantitative real-time PCR, western blot, and immunohistochemistry were subjected to measure the expression patterns of HOTAIR, STAT3, Wnt signaling factors, and epithelial-mesenchymal transition-related markers, respectively. Besides, nude mice were transplanted with colon cancer cells for further exploration. Tumor formation, volume, and weight were evaluated to validate the in vitro findings.

resultsPropofol treatment promoted cell apoptosis and inhibited cell invasion in colon cancer cells, while the effects were reversed by HOTAIR overexpression. Additionally, STAT3 positively regulated HOTAIR expression, which was also negatively modulated by propofol. Moreover, STAT3 and HOTAIR were shown to independently regulate colon cancer cell apoptosis and invasion. Furthermore, HOTAIR could stimulate Wnt signaling pathway via inhibiting WIF-1 expression and upregulating β-catenin expression, which was also demonstrated by in vivo study.

conclusionTaken together, the current study demonstrated that propofol exerts the inhibition on cell invasion and promotion on cell apoptosis through regulating STAT3/HOTAIR by activating WIF-1 and suppressing Wnt pathway, indicating that propofol might serve as a therapeutic role for colon cancer patients in the future.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsApoptosisCell Line, TumorCell MovementColonic NeoplasmsDown-RegulationGene Expression Regulation, NeoplasticHumansMiceNeoplasm InvasivenessPromoter Regions, GeneticPropofolRNA, Long NoncodingSTAT3 Transcription FactorUp-RegulationAdaptor Proteins, Signal TransducingHOTAIR long untranslated RNA, humanPropofolRNA, Long NoncodingSTAT3 protein, humanSTAT3 Transcription FactorWIF1 protein, humancolon cancerlncRNA HOTAIRpropofolSTAT3Wnt signaling

Identifiers

PMID31953926
PMCPMC7050102
OpenAlexW3000678056

What OpenQuestion holds

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LicenceCC BY
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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.