Evidence map›Paper›PMID 32218852›Full record

ArticleOncology letters2020

Pristimerin inhibits the proliferation of HT1080 fibrosarcoma cells by inducing apoptosis.

Daichi Hayashi, Toshiharu Shirai, Ryu Terauchi, Shinji Tsuchida, Naoki Mizoshiri, Yuki Mori, Yuji Arai, Osam Mazda, Toshikazu Kubo

Open access · diamondAbstract read
In one paragraph

Article in Oncology letters, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.8field-weighted citation impact, top 31% 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

5 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
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 1 institution in 1 country.

Daichi HayashiDepartment of Orthopedics, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan.
Toshiharu ShiraiDepartment of Orthopedics, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan.
Ryu TerauchiDepartment of Orthopedics, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan.
Shinji TsuchidaDepartment of Orthopedics, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan.
Naoki MizoshiriDepartment of Orthopedics, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan.
Yuki MoriDepartment of Orthopedics, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan.
Yuji AraiDepartment of Sports and Parasports Medicine, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan.
Osam MazdaDepartment of Immunology, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan.
Toshikazu KuboDepartment of Orthopedics, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan.
Kyoto Prefectural University of Medicine · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibrosarcoma is a soft tissue sarcoma that is classified as a rare cancer. Therefore, no standard anti-tumor drug therapy has been established for fibrosarcoma. Although pristimerin (PM) has been reported to exert an anti-tumor effect on various types of cancer, no studies have examined the therapeutic effect of PM on soft tissue sarcoma. The purpose of the current study was to investigate the anti-tumor effect of PM on human fibrosarcoma cells (HT1080). The present study examined the cell viability, IC50 values and ability to induce apoptosis of PM in HT1080 and normal human dermal fibroblast (aHDF) cells. The effect of PM on the following signaling pathways associated with cell proliferation was also evaluated: AKT and mitogen-activated protein kinase (MAPK). Using mice subcutaneously transplanted with fibrosarcoma cells, the effect of PM treatment was investigated on tumor growth inhibition, body weight and liver and renal function. The results revealed that PM administration reduced cell viability and induced apoptosis in a dose-dependent matter. In HT1080 cells, the IC50 value of PM was 0.16 µM at 24 h and 0.13 µM at 48 h. PM treatment also decreased the levels of phosphorylated AKT, mTOR, NF-κB and phosphorylated ERK in a dose-dependent manner. In the PM injection group, the increase in tumor volume was significantly reduced and the effect on weight loss and liver and renal function were revealed to be insignificant. PM exerted little effect on normal human dermal fibroblasts and was highly effective against human fibrosarcoma cells. The results indicated that PM may be used as a potential therapeutic agent against fibrosarcoma.

Indexed as

AKTapoptosiscaspasefibrosarcomamitogen-activated protein kinasepristimerinproliferation

Identifiers

PMID32218852
PMCPMC7068646
OpenAlexW3008058604

What OpenQuestion holds

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Read underepoch 390

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.