Modulation and function of Pumilio proteins in cancer

Silva, Isabelle Leticia Zaboroski; Kohat, Arissa Andreina; Shiguno, Patrícia

doi:10.1016/j.semcancer.2022.03.010

“… 23 As per our findings, PUM1 was upregulated in breast cancer lineage cells and tissues. 24 The encoded protein of this gene consists of eight repeats and N- and C-terminal flanking regions to form a sequence-specific RNA binding domain that acts as a post-transcriptional repressor by binding to the 3’-UTR of mRNA targets where the Pumilio Response Element (PRE), 5’-UGUANAUA-3’ leading to translational inhibition and mRNA degradation. PUM1 targets 48 genes such as DNA polymerase processivity factor proliferating cell nuclear antigen ( PCNA ) and Ubiquitin-conjugating enzyme E2 A ( UBE2A ) which are related to DNA repair and apoptosis, therefore decreasing the expression of PMUI by mediating its methylated prompter could be induced increasing its target gene expression and enhancing apoptosis and responding to anti-cancer drugs, such as cisplatin.…”

Section: Discussionmentioning

confidence: 99%

“… 25 Research in this area has shown that PUM1 is overexpressed in breast cancer lineage cells and tissues. 24 …”

Section: Discussionmentioning

confidence: 99%

Promoter Methylation-Regulated Differentially Expressed Genes in Breast Cancer

Sindi¹,

Hamdi²,

Hassan³

et al. 2023

BCTT

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Background Breast cancer is one of the most common malignancies among women. Recent studies revealed that differentially methylated regions (DMRs) are implicated in regulating gene expression. The goal of this research was to determine which genes and pathways are dysregulated in breast cancer when their promoters are methylated in an abnormal way, leading to differential expression. Whole-genome bisulfite sequencing was applied to analyze DMRs for eight peripheral blood samples collected from five Saudi females diagnosed with stages I and II of breast cancer aligned with three normal females. Three of those patients and three normal samples were used to determine differentially expressed genes (DEG) using Illumina platform NovaSeq PE150. Results Based on ontology (GO) and KEGG pathways, the analysis indicated that DMGs and DEG are closely related to associated processes, such as ubiquitin-protein transferase activity, ubiquitin-mediated proteolysis, and oxidative phosphorylation. The findings indicated a potentially significant association between global hypomethylation and breast cancer in Saudi patients. Our results revealed 81 differentially promoter-methylated and expressed genes. The most significant differentially methylated and expressed genes found in gene ontology (GO) are pumilio RNA binding family member 1 ( PUM1 ) and zinc finger AN1-type containing 2B ( ZFAND2B ) also known as ( AIRAPL ). Conclusion The essential outcomes of this study suggested that aberrant hypermethylation at crucial genes that have significant parts in the molecular pathways of breast cancer could be used as a potential prognostic biomarker for breast cancer.

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“…PUM1 is critical for MSC self-renewal and proliferation, while PUM2 represses the osteogenic differentiation of MSCs by inhibiting JAK2 and RUNX2 mRNAs [65]. Since cancer stem cells have similar characteristics, several studies have highlighted the novel function of PUM1 in cancer stem cells and cancer progression [70][71][72]. For example, Pumilio proteins promote colorectal cancer progression by inhibiting the expression of p21 mRNA [73].…”

Section: Puf Rna-binding Proteinsmentioning

confidence: 99%

C. elegans Germline as Three Distinct Tumor Models

Jones,

Norman,

Tiet

et al. 2024

Preprint

0

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Tumor cells display abnormal growth and division, avoiding the natural process of cell death. These cells can be benign (non-cancerous growth) or malignant (cancerous growth). Over the past few decades, numerous in vitro or in vivo tumor models have been employed to understand the molecular mechanisms associated with tumorigenesis in diverse aspects. However, our comprehension of how non-tumor cells transform into tumor cells at molecular and cellular levels remains incomplete. The nematode C. elegans has emerged as an excellent model organism for exploring various phenomena, including tumorigenesis. Although C. elegans does not naturally develop cancer, it serves as a valuable platform for identifying oncogenes and the underlying mechanisms within a live organism. In this review, we describe three distinct germline tumor models in C. elegans, highlighting their associated mechanisms and related regulators. Given the conservation of many of the regulators implicated in C. elegans tumorigenesis, it is proposed that these unique models hold significant potential for enhancing our comprehension of the broader control mechanisms governing tumorigenesis.

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“…PUM1 is critical for MSC self-renewal and proliferation, while PUM2 represses the osteogenic differentiation of MSCs by inhibiting JAK2 and RUNX2 mRNAs [ 72 ]. Since cancer stem cells have similar characteristics, several studies have highlighted the novel function of PUM1 in cancer stem cells and cancer progression [ 76 , 77 , 78 ]. For example, Pumilio proteins promote colorectal cancer progression by inhibiting the expression of p21 mRNA [ 79 ].…”

Section: Puf-8-loss-mediated Tumorigenesis: Spermatogenic Dedifferent...mentioning

confidence: 99%

C. elegans Germline as Three Distinct Tumor Models

Jones,

Norman,

Tiet

et al. 2024

Biology

0

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Tumor cells display abnormal growth and division, avoiding the natural process of cell death. These cells can be benign (non-cancerous growth) or malignant (cancerous growth). Over the past few decades, numerous in vitro or in vivo tumor models have been employed to understand the molecular mechanisms associated with tumorigenesis in diverse regards. However, our comprehension of how non-tumor cells transform into tumor cells at molecular and cellular levels remains incomplete. The nematode C. elegans has emerged as an excellent model organism for exploring various phenomena, including tumorigenesis. Although C. elegans does not naturally develop cancer, it serves as a valuable platform for identifying oncogenes and the underlying mechanisms within a live organism. In this review, we describe three distinct germline tumor models in C. elegans, highlighting their associated mechanisms and related regulators: (1) ectopic proliferation due to aberrant activation of GLP-1/Notch signaling, (2) meiotic entry failure resulting from the loss of GLD-1/STAR RNA-binding protein, (3) spermatogenic dedifferentiation caused by the loss of PUF-8/PUF RNA-binding protein. Each model requires the mutations of specific genes (glp-1, gld-1, and puf-8) and operates through distinct molecular mechanisms. Despite these differences in the origins of tumorigenesis, the internal regulatory networks within each tumor model display shared features. Given the conservation of many of the regulators implicated in C. elegans tumorigenesis, it is proposed that these unique models hold significant potential for enhancing our comprehension of the broader control mechanisms governing tumorigenesis.

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Modulation and function of Pumilio proteins in cancer

Cited by 8 publications

References 63 publications

Promoter Methylation-Regulated Differentially Expressed Genes in Breast Cancer

Promoter Methylation-Regulated Differentially Expressed Genes in Breast Cancer

C. elegans Germline as Three Distinct Tumor Models

C. elegans Germline as Three Distinct Tumor Models

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