Evidence map›Paper›PMID 25418289›Full record

ArticleScientific reports2014

Modulation of specificity protein 1 by mithramycin A as a novel therapeutic strategy for cervical cancer.

Eun-Sun Choi, Jeong-Seok Nam, Ji-Youn Jung, Nam-Pyo Cho, Sung-Dae Cho

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

54 citing papers in PubMed, 93 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

5 authors at 4 institutions in 1 country.

Eun-Sun ChoiDivision of High-risk Pathogen Research, Korea Centers for Disease Control and Prevention, Osong, Republic of Korea.
Jeong-Seok NamLee Gil Ya Cancer and Diabetes Institute, Gachon University, Graduate School of Medicine, Incheon 406-840, Korea.
Ji-Youn JungDepartment of Companion and Laboratory Animal Science, Kongju National University, Yesan 314-701, Republic of Korea.
Nam-Pyo ChoDepartment of Oral Pathology, School of Dentistry and Institute of Biodegradable Material, Institute of Oral Bioscience, Brain Korea 21 Project, Chonbuk National University, Jeon-ju 561-756, Republic of Korea.
Sung-Dae ChoDepartment of Oral Pathology, School of Dentistry and Institute of Biodegradable Material, Institute of Oral Bioscience, Brain Korea 21 Project, Chonbuk National University, Jeon-ju 561-756, Republic of Korea.
Gachon University · KRJeonbuk National University · KRKongju National University · KRKorea Center for Disease Control and Prevention · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cervical cancer is the third most common cancer and the third leading cause of death among women. However, the standard treatment for cervical cancer includes cisplatin, which can cause side effects such as hematological damage or renal toxicity. New innovations in cervical cancer treatment focus on developing more effective and better-tolerated therapies such as Sp1-targeting drugs. Previous studies suggested that mithramycin A (Mith) inhibits the growth of various cancers by decreasing Sp1 protein. However, how Sp1 protein is decreased by Mith is not clear. Few studies have investigated the regulation of Sp1 protein by proteasome-dependent degradation as a possible control mechanism for the regulation of Sp1 in cancer cells. Here, we show that Mith decreased Sp1 protein by inducing proteasome-dependent degradation, thereby suppressing cervical cancer growth through a DR5/caspase-8/Bid signaling pathway. We found that prolonged Mith treatment was well tolerated after systemic administration to mice carrying cervical cancer cells. Reduction of body weight was minimal, indicating that Mith was a good therapeutic candidate for treatment of cancers in which Sp1 is involved in promoting and developing disease.

Indexed as

AnimalsAntibiotics, AntineoplasticApoptosisBH3 Interacting Domain Death Agonist ProteinCaspase 8Cell Line, TumorCell ProliferationFemaleHumansMembrane Potential, MitochondrialMiceMice, NudeMitochondriaPeptide HydrolasesPlicamycinReceptors, TNF-Related Apoptosis-Inducing LigandAntibiotics, AntineoplasticBH3 Interacting Domain Death Agonist ProteinCaspase 8mithramycin APeptide HydrolasesPlicamycinReceptors, TNF-Related Apoptosis-Inducing LigandSP1 protein, humanSp1 Transcription Factor

Identifiers

PMID25418289
PMCPMC4241519
OpenAlexW2022595078

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.