Evidence map›Paper›PMID 38523637›Full record

ReviewFrontiers in pharmacology2024

AKR1C3 in carcinomas: from multifaceted roles to therapeutic strategies.

Mengnan Li, Limin Zhang, Jiahui Yu, Xiaoxiao Wang, Le Cheng, Zhaowu Ma, Xiaoguang Chen, Lingzhi Wang, Boon Cher Goh

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in pharmacology, 2024. 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
7.5field-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, 23 citations in OpenAlex.

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  16. Unveiling the Bioactive Efficacy ofPharmaceuticals (Basel, Switzerland) · 2024
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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

9 authors at 3 institutions in 2 countries.

Mengnan LiSchool of Basic Medicine, Health Science Center, Yangtze University, Jingzhou, China.
Limin ZhangJingzhou Hospital of Traditional Chinese Medicine, Jingzhou, China.
Jiahui YuSchool of Basic Medicine, Health Science Center, Yangtze University, Jingzhou, China.
Xiaoxiao WangSchool of Basic Medicine, Health Science Center, Yangtze University, Jingzhou, China.
Le ChengSchool of Basic Medicine, Health Science Center, Yangtze University, Jingzhou, China.
Zhaowu MaSchool of Basic Medicine, Health Science Center, Yangtze University, Jingzhou, China.
Xiaoguang ChenSchool of Basic Medicine, Health Science Center, Yangtze University, Jingzhou, China.
Lingzhi WangDepartment of Haematology-Oncology, National University Cancer Institute, Singapore, Singapore.
Boon Cher GohDepartment of Haematology-Oncology, National University Cancer Institute, Singapore, Singapore.
Yangtze University · CNNational University Cancer Institute, Singapore · SGNational University of Singapore · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aldo-Keto Reductase Family 1 Member C3 (AKR1C3), also known as type 5 17β-hydroxysteroid dehydrogenase (17β-HSD5) or prostaglandin F (PGF) synthase, functions as a pivotal enzyme in androgen biosynthesis. It catalyzes the conversion of weak androgens, estrone (a weak estrogen), and PGD2 into potent androgens (testosterone and 5α-dihydrotestosterone), 17β-estradiol (a potent estrogen), and 11β-PGF2α, respectively. Elevated levels of AKR1C3 activate androgen receptor (AR) signaling pathway, contributing to tumor recurrence and imparting resistance to cancer therapies. The overexpression of AKR1C3 serves as an oncogenic factor, promoting carcinoma cell proliferation, invasion, and metastasis, and is correlated with unfavorable prognosis and overall survival in carcinoma patients. Inhibiting AKR1C3 has demonstrated potent efficacy in suppressing tumor progression and overcoming treatment resistance. As a result, the development and design of AKR1C3 inhibitors have garnered increasing interest among researchers, with significant progress witnessed in recent years. Novel AKR1C3 inhibitors, including natural products and analogues of existing drugs designed based on their structures and frameworks, continue to be discovered and developed in laboratories worldwide. The AKR1C3 enzyme has emerged as a key player in carcinoma progression and therapeutic resistance, posing challenges in cancer treatment. This review aims to provide a comprehensive analysis of AKR1C3's role in carcinoma development, its implications in therapeutic resistance, and recent advancements in the development of AKR1C3 inhibitors for tumor therapies.

Indexed as

AKR1C3carcinoma progressioncombination therapiesinhibitorstherapeutic resistance

Identifiers

PMID38523637
PMCPMC10957692
OpenAlexW4392592704

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.