Evidence map›Paper›PMID 33846813›Full record

ArticleOncology reports2021

Celastrol attenuates the inflammatory response by inhibiting IL‑1β expression in triple‑negative breast cancer cells.

Daeun You, Yisun Jeong, Sun Young Yoon, Sung A Kim, Seok Won Kim, Seok Jin Nam, Jeong Eon Lee, Sangmin Kim

Open access · hybridAbstract read
In one paragraph

Article in Oncology reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
8.2field-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

16 citing papers in PubMed, 37 citations in OpenAlex.

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  12. Native Endophytes ofFrontiers in microbiology · 2022
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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

8 authors at 3 institutions in 1 country.

Daeun You *Department of Health Sciences and Technology, The Samsung Advanced Institute for Health Sciences and Technology, Sungkyunkwan University, Seoul 06351, Republic of Korea.
Yisun Jeong *Department of Health Sciences and Technology, The Samsung Advanced Institute for Health Sciences and Technology, Sungkyunkwan University, Seoul 06351, Republic of Korea.
Sun Young YoonDepartment of Health Sciences and Technology, The Samsung Advanced Institute for Health Sciences and Technology, Sungkyunkwan University, Seoul 06351, Republic of Korea.
Sung A KimDepartment of Health Sciences and Technology, The Samsung Advanced Institute for Health Sciences and Technology, Sungkyunkwan University, Seoul 06351, Republic of Korea.
Seok Won KimDepartment of Breast Cancer Center, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul 06351, Republic of Korea.
Seok Jin NamDepartment of Breast Cancer Center, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul 06351, Republic of Korea.
Jeong Eon LeeDepartment of Health Sciences and Technology, The Samsung Advanced Institute for Health Sciences and Technology, Sungkyunkwan University, Seoul 06351, Republic of Korea.
Sangmin KimDepartment of Breast Cancer Center, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul 06351, Republic of Korea.
Samsung Medical Center · KRSamsung (South Korea) · KRSungkyunkwan University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

IL‑1 promotes cancer cell proliferation and invasiveness in various malignancies, such as breast and colorectal cancer. In the present study, the functional roles of IL‑1β (IL1B) and the inhibitory effect of celastrol on IL1B expression were investigated in triple‑negative breast cancer (TNBC) cells. The data revealed that celastrol markedly decreased IL1B expression and suppressed TNBC cell proliferation in a dose‑dependent manner. The levels of IL1B and IL8 mRNA were significantly increased in TNBC cells compared with non‑TNBC cells. In addition, IL1B augmented the expression levels of IL8 as well as matrix metalloproteinases (MMPs), including MMP‑1 and MMP‑9, in TNBC cells. Furthermore, IL1B expression was decreased by a specific MEK1/2 inhibitor, MEK162. Celastrol also promoted IL1B downregulation through the suppression of the MEK/ERK‑dependent pathway. Furthermore, the results also revealed a decrease in IL1B‑induced IL8, MMP‑1, and MMP‑9 expression in response to celastrol treatment. The induction of cellular invasion by IL1B was also markedly decreased by celastrol. Collectively, the present study results suggested celastrol as an effective drug for the treatment of TNBC, involving a reduction in IL1B expression, activity or signaling pathways.

Indexed as

BenzimidazolesCell Line, TumorCell MovementCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansInterleukin-1betaMAP Kinase Signaling SystemNeoplasm InvasivenessPentacyclic TriterpenesTriple Negative Breast NeoplasmsBenzimidazolesbinimetinibcelastrolIL1B protein, humanInterleukin-1betaPentacyclic Triterpenescelastrolinterleukin 1βinterleukin 8matrix metalloproteinase 1matrix metalloproteinase 9triple‑negative breast cancer

Identifiers

PMID33846813
PMCPMC8042664
OpenAlexW3144120187

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.