MALAT1 promotes FOXA1 degradation by competitively binding to miR-216a-5p and enhancing neuroendocrine differentiation in prostate cancer

Zeng, Fanchang; Li, Daoyuan; Kang, Xinli; Wu, Qinghui; Song, Mi; Ou, Zhewen; Yang, Zuobing; Yang, Jing; Luo, Liumei

doi:10.1016/j.tranon.2023.101807

Cited by 4 publications

(1 citation statement)

References 64 publications

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“…Additionally, Foxa1/2's regulation of genes associated with neuroendocrine cell identity implies that damage to these transcription factors could lead to altered expression of neuroendocrine markers, impacting the identity and functional properties of small intestinal neuroendocrine cells [54]. The in uence of Foxa1/2 on genes involved in hormone production by endocrine cells is another signi cant aspect.…”

Section: Pdx1mentioning

confidence: 99%

Investigating Carcinoid Tumor Oncogenesis through the lens of Developmental Dynamics involved in Small Intestinal Neuroendocrine Cells

Shafi,

Yaqub

2024

Preprint

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Background: Carcinoid tumors from small intestinal Neuroendocrine Cells (SI-NECs) present clinical challenges with increasing incidence. Investigating the genetic architecture is crucial, as dysregulation in transcription factors and signaling pathways contributes to aberrant behavior, including uncontrolled proliferation and hormone secretion. Understanding these mechanisms holds promise for identifying therapeutic targets and biomarkers, not only for carcinoid tumors but also for broader applications in neuroendocrine neoplasms and gastrointestinal malignancies. Methods: Databases, including PubMed, MEDLINE, Google Scholar, and open access/subscription-based journals were searched for published articles without any date restrictions, to investigate the intricate genetic architecture and developmental dynamics underlying the development of carcinoid tumors originating from small intestinal Neuroendocrine Cells (SI-NECs). Based on the criteria mentioned in the methods section, studies were systematically reviewed to investigate carcinoid tumor oncogenesis. This study adheres to relevant PRISMA guidelines (Preferred Reporting Items for Systematic Reviews and Meta-Analyses). Results: This investigation into the genetic architecture of small intestinal neuroendocrine cells (SI-NECs) reveals intricate dysregulations contributing to carcinoid tumor development. Dysfunctional expression of key transcription factors, including Neurogenin 3, Pdx1, Isl1, Foxa1/2, Hes1, and others, disrupts neuroendocrine differentiation, impacting hormone expression profiles. Chromogranin A dysregulation affects the maturation of SI-NECs, while alterations in Delta-like 1/4 and serotonin contribute to abnormal behavior. Dysfunctional Tcf4 and Gfi1b influence cell fate decisions, and NeuroD1 alterations impact maturation. Dysregulation of GATA factors, Nkx2.2, Sox factors, and Neurotrophins further complicates SI-NECs. Protein Kinase A signaling dysregulation contributes to uncontrolled proliferation. These findings advance our understanding of the complexity of carcinoid tumor development, possibly providing a framework for targeted therapeutic strategies addressing the specific aberrations identified in SI-NECs. Conclusion: The dysregulation in the genetic architecture of small intestinal Neuroendocrine Cells (SI-NECs) precipitates carcinoid tumor development. Alterations in key transcription factors, signaling pathways, and developmental processes disrupt neuroendocrine differentiation, hormone expression, and cell fate determination. Dysfunctional molecular cascades including Notch and Wnt signaling drive uncontrolled proliferation and aberrant hormone secretion characteristic of carcinoid tumors. Understanding the intricate molecular landscape of SI-NEC dysregulation is paramount for targeted therapies. Insights emerging from this research may pave the way for novel interventions aimed at mitigating carcinoid tumor progression and improving patient outcomes.

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Section: Pdx1mentioning

confidence: 99%

Investigating Carcinoid Tumor Oncogenesis through the lens of Developmental Dynamics involved in Small Intestinal Neuroendocrine Cells

Shafi,

Yaqub

2024

Preprint

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Exploring the tumor genomic landscape of aggressive prostate cancer by whole‐genome sequencing of tissue or liquid biopsies

Weiss,

Lamy,

Rusan

et al. 2024

Intl Journal of Cancer

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Treatment resistance remains a major issue in aggressive prostate cancer (PC), and novel genomic biomarkers may guide better treatment selection. Circulating tumor DNA (ctDNA) can provide minimally invasive information about tumor genomes, but the genomic landscape of aggressive PC based on whole‐genome sequencing (WGS) of ctDNA remains incompletely characterized. Thus, we here performed WGS of tumor tissue (n = 31) or plasma ctDNA (n = 10) from a total of 41 aggressive PC patients, including 11 hormone‐naïve, 15 hormone‐sensitive, and 15 castration‐resistant patients. Across all variant types, we found progressively more altered tumor genomic profiles in later stages of aggressive PC. The potential driver genes most frequently affected by single‐nucleotide variants or insertions/deletions included the known PC‐related genes TP53, CDK12, and PTEN and the novel genes COL13A1, KCNH3, and SENP3. Etiologically, aggressive PC was associated with age‐related and DNA repair‐related mutational signatures. Copy number variants most frequently affected 14q11.2 and 8p21.2, where no well‐recognized PC‐related genes are located, and also frequently affected regions near the known PC‐related genes MYC, AR, TP53, PTEN, and BRCA1. Structural variants most frequently involved not only the known PC‐related genes TMPRSS2 and ERG but also the less extensively studied gene in this context, PTPRD. Finally, clinically actionable variants were detected throughout all stages of aggressive PC and in both plasma and tissue samples, emphasizing the potential clinical applicability of WGS of minimally invasive plasma samples. Overall, our study highlights the feasibility of using liquid biopsies for comprehensive genomic characterization as an alternative to tissue biopsies in advanced/aggressive PC.

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Innovations in Metal-Based Nanomedicines to Interfere with the Signaling Communications of Prostate Cancer

Habeeb,

Deepthi,

Vengateswaran

et al. 2024

BioNanoSci.

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MALAT1 promotes FOXA1 degradation by competitively binding to miR-216a-5p and enhancing neuroendocrine differentiation in prostate cancer

Cited by 4 publications

References 64 publications

Investigating Carcinoid Tumor Oncogenesis through the lens of Developmental Dynamics involved in Small Intestinal Neuroendocrine Cells

Investigating Carcinoid Tumor Oncogenesis through the lens of Developmental Dynamics involved in Small Intestinal Neuroendocrine Cells

Exploring the tumor genomic landscape of aggressive prostate cancer by whole‐genome sequencing of tissue or liquid biopsies

Innovations in Metal-Based Nanomedicines to Interfere with the Signaling Communications of Prostate Cancer

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