ArticleFEBS open bio2019
LKB1 suppresses androgen synthesis in a mouse model of hyperandrogenism via IGF-1 signaling.
Article in FEBS open bio, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 4 papers.
What it found
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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.
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.
Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Insights into targeting LKB1 in tumorigenesis.Genes & diseases · 2025Review
- Salt-inducible kinases regulate androgen synthesis in theca cells by enhancing CREB signaling.Molecular and cellular endocrinology · 2023Article
- Improvement Effect of Metformin on Female and Male Reproduction in Endocrine Pathologies and Its Mechanisms.Pharmaceuticals (Basel, Switzerland) · 2021Review
- The Association Between Polycystic Ovary Syndrome and Its Dermatological Manifestations.Cureus · 2020Review
Corrections and comments
- Retraction · 2024-12-06Duplication of/in Image · Investigation by Journal/Publisher · Investigation by Third Party · Unreliable Results and/or Conclusions ·
- Retracted
Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polycystic ovary syndrome (PCOS) is a major cause of anovulatory sterility in women, and most PCOS patients exhibit hyperandrogenism (HA). Liver kinase b1 (LKB1) is a tumor suppressor that has recently been reported to be involved in PCOS. However, the mechanism by which LKB1 affects HA has not previously been elucidated. We report here that ovarian LKB1 levels are significantly decreased in a female mouse model of HA. Moreover, we report that LKB1 expression is inhibited by elevated androgens via activation of androgen receptors. In addition, LKB1 treatment was observed to suppress androgen synthesis in theca cells and promote estrogen production in granulosa cells by regulating steroidogenic enzyme expression. As expected, LKB1 knockdown inhibited estrogen levels and enhanced androgen levels, and LKB1-transgenic mice were protected against HA. The effect of LKB1 appears to be mediated via IGF-1 signaling. In summary, we describe here a key role for LKB1 in controlling sex hormone levels.
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Registered trials
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 Socratic graph.