Anti-Cancer Effect of Lambertianic Acid by Inhibiting the AR in LNCaP Cells

Lee, Myoung-Sun; Lee, Seon-Ok; Kim, Ju‐Ha; Lee, Eun-Ok; Lee, Hyo‐Jeong

doi:10.3390/ijms17071066

Cited by 10 publications

(8 citation statements)

References 31 publications

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“…Decreased AR signaling leads to apoptosis via activation of Caspase-3. 52 This decreased AR signaling might lead to sPTB via apoptosis of the fetal membrane in the placenta. 53 In addition, interactions of IGF1 and AR genes may affect the onset of spontaneous preterm labor.…”

Section: Genome-wide Linkage Studiesmentioning

confidence: 99%

Genetics, epigenetics, and transcriptomics of preterm birth

Jain

Monangi

Zhang

et al. 2022

American J Rep Immunol

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Preterm birth contributes significantly to neonatal mortality and morbidity. Despite its global significance, there has only been limited progress in preventing preterm birth. Spontaneous preterm birth (sPTB) results from a wide variety of pathological processes. Although many non‐genetic risk factors influence the timing of gestation and labor, compelling evidence supports the role of substantial genetic and epigenetic influences and their interactions with the environment contributing to sPTB. To investigate a common and complex disease such as sPTB, various approaches such as genome‐wide association studies, whole‐exome sequencing, transcriptomics, and integrative approaches combining these with other ‘omics studies have been used. However, many of these studies were typically small or focused on a single ethnicity or geographic region with limited data, particularly in populations at high risk for sPTB, or lacked a robust replication. These studies found many genes involved in the inflammation and immunity‐related pathways that may affect sPTB. Recent studies also suggest the role of epigenetic modifications of gene expression by the environmental signals as a potential contributor to the risk of sPTB. Future genetic studies of sPTB should continue to consider the contributions of both maternal and fetal genomes as well as their interaction with the environment.

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Section: Genome-wide Linkage Studiesmentioning

confidence: 99%

Genetics, epigenetics, and transcriptomics of preterm birth

Jain

Monangi

Zhang

et al. 2022

American J Rep Immunol

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“…Interestingly, it had been suggested earlier that molecular crosstalk between IGF1R and AR might lead to sPTB 21 . Later studies have shown that a longer polyglutamine chain in the N-terminal transactivation domain of AR hinders transactivation activity 22 resulting in decreased AR signaling which leads to apoptosis via activation of Caspase-3 23 . Since apoptosis in the placenta is involved in sPTB 24 , decreased AR signaling might lead to sPTB via apoptosis in the placenta.…”

Section: Genomic Approaches To Study Sptbmentioning

confidence: 99%

Spontaneous preterm birth: the underpinnings in the maternal and fetal genomes

Bhattacharjee

Maitra

2021

npj Genom. Med.

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Preterm birth (PTB) is a major cause of neonatal mortality and health complications in infants. Elucidation of its genetic underpinnings can lead to improved understanding of the biological mechanisms and boost the development of methods to predict PTB. Although recent genome-based studies of both mother and fetus have identified several genetic loci which might be implicated in PTB, these results suffer from a lack of consistency across multiple studies and populations. Moreover, results of functional validation of most of these findings are unavailable. Since medically indicated preterm deliveries have well-known heterogeneous causes, we have reviewed only those studies which investigated spontaneous preterm birth (sPTB) and have attempted to suggest probable biological mechanisms by which the implicated genetic factors might result in sPTB. We expect our review to provide a panoramic view of the genetics of sPTB.

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“…Lambertianic acid (LA; Figure 1a), a major component of Pinus koraiensis , was known to have anti-obesity [18], anti-inflammatory [19], and anti-cancer effects [20,21,22]. Nevertheless, the underlying molecular mechanisms of LA were not fully understood in association with STAT3 phosphorylation and RelA/p65 acetylation.…”

Section: Introductionmentioning

confidence: 99%

Suppression of STAT3 Phosphorylation and RelA/p65 Acetylation Mediated by MicroRNA134 Plays a Pivotal Role in the Apoptotic Effect of Lambertianic Acid

Sim

Lee

Jung

et al. 2019

IJMS

Self Cite

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As p300-mediated RelA/p65 hyperacetylation by signal transducers and activators of transcription 3 (STAT3) is critical for NF-κB activation, in the current study, the apoptotic mechanism of lambertianic acid (LA) was explored in relation to STAT3 phosphorylation and RelA/p65 acetylation in MCF-7, DU145, PC-3, and MDA-MB-453 cells. LA significantly increased the cytotoxicity, sub G 1 population, and the cleavage of poly (ADP-ribose) polymerase (PARP) in MDA-MB-453 or PC-3 cells (STAT3 mutant), more than in the MCF-7 or DU145 cells (STAT3 wild). Consistently, LA inhibited the phosphorylation of STAT3 and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), and disrupted the interaction between p-STAT3, p300, NF-κB, and RelA/p65 acetylation (Ac-RelA/p65) in the MCF-7 and DU145 cells. Also, LA reduced the nuclear translocation of STAT3 and NF-κB via their colocalization, and also suppressed the protein expression of XIAP, survivin, Bcl-2, Bcl-xL, vascular endothelial growth factor (VEGF), Cox-2, c-Myc and mRNA expression of interleukin 6 (IL-6), and tumor necrosis factor-α (TNF-α) in MCF-7 cells. Conversely, IL-6 blocked the ability of LA to suppress the cytotoxicity and PARP cleavage, while the depletion of STAT3 or p300 enhanced the PARP cleavage of LA in the MCF-7 cells. Notably, LA upregulated the level of miRNA134 and so miRNA134 mimic attenuated the expression of pro-PARP, p-STAT3, and Ac-RelA, while the miRNA134 inhibitor reversed the ability of LA to reduce the expression of Ac-RelA and pro-PARP in MCF-7 cells. Overall, these findings suggest that LA induced apoptosis via the miRNA-134 mediated inhibition of STAT3 and RelA/p65 acetylation.

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Anti-Cancer Effect of Lambertianic Acid by Inhibiting the AR in LNCaP Cells

Cited by 10 publications

References 31 publications

Genetics, epigenetics, and transcriptomics of preterm birth

Genetics, epigenetics, and transcriptomics of preterm birth

Spontaneous preterm birth: the underpinnings in the maternal and fetal genomes

Suppression of STAT3 Phosphorylation and RelA/p65 Acetylation Mediated by MicroRNA134 Plays a Pivotal Role in the Apoptotic Effect of Lambertianic Acid

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