Role of Plexin B1 in a Breast Cancer Cohort of Pakistani Patients and its Contribution Towards Cancer Metastasis as Indicated by an In Vitro Model

Malik, Muhammad Ehsan; Riaz, Syeda Kiran; Waqar, SH; Faq, Farhan; Ye, Lin; Jiang, Wen Guo

doi:10.21873/anticanres.11844

Cited by 2 publications

(2 citation statements)

References 17 publications

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“…KCNIP1 is an important component of potassium channel complexes, which regulates neuronal membrane excitability 47,48 . PLXNB1 is involved in extensive biological processes including cell adhesion, cell migration, and cell shape regulation [49][50][51][52] . OGDHL is a component of the oxoglutarate dehydrogenase complex that is involved in degradation of glucose and glutamate, and has been associated with tumor development and progression 53,54 .…”

Section: Discussionmentioning

confidence: 99%

Former smoking associated with epigenetic modifications in human granulosa cells among women undergoing assisted reproduction

Tang,

Gaskins,

Hood

et al. 2024

Sci Rep

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Smoking exposure during adulthood can disrupt oocyte development in women, contributing to infertility and possibly adverse birth outcomes. Some of these effects may be reflected in epigenome profiles in granulosa cells (GCs) in human follicular fluid. We compared the epigenetic modifications throughout the genome in GCs from women who were former (N = 15) versus never smokers (N = 44) undergoing assisted reproductive technologies (ART). This study included 59 women undergoing ART. Smoking history including time since quitting was determined by questionnaire. GCs were collected during oocyte retrieval and DNA methylation (DNAm) levels were profiled using the Infinium MethylationEPIC BeadChip. We performed an epigenome-wide association study with robust linear models, regressing DNAm level at individual loci on smoking status, adjusting for age, ovarian stimulation protocol, and three surrogate variables. We performed differentially methylated regions (DMRs) analysis and over-representation analysis of the identified CpGs and corresponding gene set. 81 CpGs were differentially methylated among former smokers compared to never smokers (FDR < 0.05). We identified 2 significant DMRs (KCNQ1 and RHBDD2). The former smoking-associated genes were enriched in oxytocin signaling, adrenergic signaling in cardiomyocytes, platelet activation, axon guidance, and chemokine signaling pathway. These epigenetic variations have been associated with inflammatory responses, reproductive outcomes, cancer development, neurodevelopmental disorder, and cardiometabolic health. Secondarily, we examined the relationships between time since quitting and DNAm at significant CpGs. We observed three CpGs in negative associations with the length of quitting smoking (p < 0.05), which were cg04254052 (KCNIP1), cg22875371 (OGDHL), and cg27289628 (LOC148145), while one in positive association, which was cg13487862 (PLXNB1). As a pilot study, we demonstrated epigenetic modifications associated with former smoking in GCs. The study is informative to potential biological pathways underlying the documented association between smoking and female infertility and biomarker discovery for smoking-associated reproductive outcomes.

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Section: Discussionmentioning

confidence: 99%

Former smoking associated with epigenetic modifications in human granulosa cells among women undergoing assisted reproduction

Tang,

Gaskins,

Hood

et al. 2024

Sci Rep

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“…Opposite results were reported in a study that examined the role of plexin-B1 in breast cancer metastasis. In that study, knockdown of plexin B1 in MDA-MB-231 cells led to a remarkable increase in the motility of breast cancer cells ( Table 1 ) [ 60 ]. Plexin-B1 was also found to function as a tumor suppressor gene in primary melanoma harboring an activated Raf oncogene.…”

Section: The Role Of the Different Plexins In Tumor Progressionmentioning

confidence: 99%

Plexins as Regulators of Cancer Cell Proliferation, Migration, and Invasivity

Toledano

Neufeld

2023

Cancers

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Plexins are a family of nine single-pass transmembrane receptors with a conserved GTPase activating protein (GAP) domain. The plexin family is divided into four subfamilies: Type-A, type-B, type-C, and type-D plexins. Plexins function as receptors for axon guidance factors of the semaphorin family. The semaphorin gene family contains 22 genes that are divided into eight subclasses of which subclasses three to seven represent vertebrate semaphorins. The plexins and their semaphorin ligands have important roles as regulators of angiogenesis, cancer proliferation, and metastasis. Class 3 semaphorins, with the exception of sema3E, are the only semaphorins that do not bind directly to plexins. In order to transduce their signals, they bind instead to complexes consisting of receptors of the neuropilin family and various plexins. Some plexins also form complexes with tyrosine-kinase receptors such as the epidermal growth factor receptor ErbB2, the mesenchymal epithelial transition factor receptor (MET), and the Vascular endothelial growth factor receptor 2 (VEGFR2) and, as a result, can modulate cell proliferation and tumor progression. This review focuses on the roles of the different plexins in the control of cancer cell proliferation and invasiveness. Plexins also affect tumor progression and tumor metastasis by indirect mechanisms, such as modulation of angiogenesis and immune responses. However, these topics are not covered in the present review.

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Role of Plexin B1 in a Breast Cancer Cohort of Pakistani Patients and its Contribution Towards Cancer Metastasis as Indicated by an In Vitro Model

Abstract: Loss of plexin B1 expression might play a pivotal role in enhancing the metastatic potential of breast cancer cells.

Cited by 2 publications

References 17 publications

Former smoking associated with epigenetic modifications in human granulosa cells among women undergoing assisted reproduction

Former smoking associated with epigenetic modifications in human granulosa cells among women undergoing assisted reproduction

Plexins as Regulators of Cancer Cell Proliferation, Migration, and Invasivity

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