Evidence map›Paper›PMID 38203388›Full record

ArticleInternational journal of molecular sciences2023

Therapeutic Efficacy of YM155 to Regulate an Epigenetic Enzyme in Major Subtypes of RCC.

Seong Hwi Hong, Young Ju Lee, Eun Bi Jang, Hyun Ji Hwang, Eun Song Kim, Da Hyeon Son, Sung Yul Park, Hong Sang Moon, Young Eun Yoon

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.5field-weighted citation impact, top 32% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. Article
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.

Seong Hwi HongDepartment of Urology, Hanyang University College of Medicine, Seoul 04763, Republic of Korea.
Young Ju LeeDepartment of Urology, Hanyang University College of Medicine, Seoul 04763, Republic of Korea.
Eun Bi JangDepartment of Translational Medicine, Hanyang University Graduate School of Biomedical Science & Engineering, Seoul 04763, Republic of Korea.
Hyun Ji HwangDepartment of Translational Medicine, Hanyang University Graduate School of Biomedical Science & Engineering, Seoul 04763, Republic of Korea.
Eun Song KimDepartment of Translational Medicine, Hanyang University Graduate School of Biomedical Science & Engineering, Seoul 04763, Republic of Korea.
Da Hyeon SonDepartment of Translational Medicine, Hanyang University Graduate School of Biomedical Science & Engineering, Seoul 04763, Republic of Korea.
Sung Yul ParkDepartment of Urology, Hanyang University College of Medicine, Seoul 04763, Republic of Korea.
Hong Sang MoonDepartment of Urology, Hanyang University College of Medicine, Seoul 04763, Republic of Korea.
Young Eun YoonDepartment of Urology, Hanyang University College of Medicine, Seoul 04763, Republic of Korea.ORCID 0000-0001-8059-6649
Hanyang University · KR

Funding

Hanyang University HY-2019
6 · The paper itself

Abstract

Renal cell carcinoma (RCC) is the most common type of kidney cancer and includes more than 10 subtypes. Compared to the intensively investigated clear cell RCC (ccRCC), the underlying mechanisms and treatment options of other subtypes, including papillary RCC (pRCC) and chromogenic RCC (chRCC), are limited. In this study, we analyzed the public databases for ccRCC, pRCC, and chRCC and found that BIRC5 was commonly overexpressed in a large cohort of pRCC and chRCC patients as well as ccRCC and was closely related to the progression of RCCs. We investigated the potential of BIRC5 as a therapeutic target for these three types of RCCs. Loss and gain of function studies showed the critical role of BIRC5 in cancer growth. YM155, a BIRC5 inhibitor, induced a potent tumor-suppressive effect in the three types of RCC cells and xenograft models. To determine the mechanism underlying the anti-tumor effects of YM155, we examined epigenetic modifications in the BIRC5 promoter and found that histone H3 lysine 27 acetylation (H3K27Ac) was highly enriched on the promoter region of BIRC5. Chromatin-immunoprecipitation analysis revealed that H3K27Ac enrichment was significantly decreased by YM155. Immunohistochemistry of xenografted tissue showed that overexpression of BIRC5 plays an important role in malignancy in RCC. Furthermore, high expression of P300 was significantly associated with the progression of RCC. Our findings demonstrate the P300-H3K27Ac-BIRC5 cascade in three types of RCC and provide a therapeutic path for future research on RCC.

Indexed as

Carcinoma, Renal CellKidney NeoplasmsNaphthoquinonesEpigenesis, GeneticHumansImidazolesImidazolesNaphthoquinonesBIRC5histone acetylationrenal cell carcinomaYM155

Identifiers

PMID38203388
PMCPMC10779260
OpenAlexW4390175382

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.