Pathological role of long non-coding (lnc) RNA in the regulation of Wnt/β-catenin signaling pathway during epithelial-mesenchymal transition (EMT)

Alsaab, Hashem O.

doi:10.1016/j.prp.2023.154566

Cited by 7 publications

(4 citation statements)

References 90 publications

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“…The canonical Wnt/β-catenin signaling pathway is a key regulator of EMT and tumor progression [ 40 ]. Upon activation of the Wnt pathway, β-catenin accumulates in nuclei and leads to EMT [ 17 ]. In this study, we showed that GNAS mutations lead to increased MEG3 expression but decreased β-catenin expression.…”

Section: Discussionmentioning

confidence: 99%

“…The Wnt/β-catenin pathway plays an important role in tumorigenesis, cellular proliferation, and invasion [ 16 ]. Extensive studies have shown that lncRNAs have the potential to target canonical Wnt-related components during epithelial–mesenchymal transition (EMT) process [ 17 ]. Studies have demonstrated that MEG3 negatively regulates the Wnt/β-catenin signaling pathway in tumor growth and invasion [ 18 , 19 ].…”

Section: Introductionmentioning

confidence: 99%

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<i>GNAS</i> mutations suppress cell invasion by activating MEG3 in growth hormone–secreting pituitary adenoma

TANG,

ZHONG,

ZHU

et al. 2024

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Approximately 30%–40% of growth hormone–secreting pituitary adenomas (GHPAs) harbor somatic activating mutations in GNAS (α subunit of stimulatory G protein). Mutations in GNAS are associated with clinical features of smaller and less invasive tumors. However, the role of GNAS mutations in the invasiveness of GHPAs is unclear. GNAS mutations were detected in GHPAs using a standard polymerase chain reaction (PCR) sequencing procedure. The expression of mutation-associated maternally expressed gene 3 ( MEG3 ) was evaluated with RT-qPCR. MEG3 was manipulated in GH3 cells using a lentiviral expression system. Cell invasion ability was measured using a Transwell assay, and epithelial–mesenchymal transition (EMT)-associated proteins were quantified by immunofluorescence and western blotting. Finally, a tumor cell xenograft mouse model was used to verify the effect of MEG3 on tumor growth and invasiveness. The invasiveness of GHPAs was significantly decreased in mice with mutated GNAS compared with that in mice with wild-type GNAS . Consistently, the invasiveness of mutant GNAS -expressing GH3 cells decreased. MEG3 is uniquely expressed at high levels in GHPAs harboring mutated GNAS . Accordingly, MEG3 upregulation inhibited tumor cell invasion, and conversely, MEG3 downregulation increased tumor cell invasion. Mechanistically, GNAS mutations inhibit EMT in GHPAs. MEG3 in mutated GNAS cells prevented cell invasion through the inactivation of the Wnt/β-catenin signaling pathway, which was further validated in vivo . Our data suggest that GNAS mutations may suppress cell invasion in GHPAs by regulating EMT through the activation of the MEG3/Wnt/β-catenin signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

<i>GNAS</i> mutations suppress cell invasion by activating MEG3 in growth hormone–secreting pituitary adenoma

TANG,

ZHONG,

ZHU

et al. 2024

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“…17,18 Breast cancer has a convoluted development mechanism in addition to a high incidence rate, bad prognosis, and major effects on women's ability to lead healthy lives. 19,20 With the deepening of lncRNA research, more and more lncRNAs have been found to play important roles in breast 21,22 IncRNA UCA1 has been reported to upregulate protein tyrosine phosphatase PTP1B in breast cancer cells through adsorption of miR-206, thereby enhancing cell proliferation. 23 LncRNA NEAT1 promotes the expression of ZEB1, a key transcription factor in EMT, through competitive adsorption of miR-448, which in turn accelerates breast cancer cells invasion and metastasis.…”

Section: Discussionmentioning

confidence: 99%

Expression and Significance of LINC02418 in Breast Cancer

Zhou,

Huang

2024

BCTT

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Purpose The complicated pathogenesis and poor prognosis of breast cancer have become a major difficulty in medical research. This study aims to explore new lncRNA as prognostic markers for breast cancer and explore their roles and molecular mechanisms to lay a foundation for the treatment of cancer patients. Patients and Methods The expression of LINC02418 and miR-766-5p in breast cancer tissues and cells was first identified using polymerase chain reaction, and Pearson was used to examine the correlation between the two. The cancer cells activities under different transfection conditions were detected using the Transwell assay and CCK8 assay. The correlation between LINC02418 and patient prognosis was analyzed using multifactor Cox regression and Kaplan-Meier. Results It was shown that LINC02418 expression was upregulated in breast cancer tissues and cells. There are significant differences in lymph node metastasis and TNM stage between high and low LINC02418 expression groups. The higher the expression of LINC02418, the higher the mortality rate of breast cancer patients. miR-766-5p expression was downregulated and negatively correlated with LINC02418. There are binding sites between LINC02418 and miR-766-5p; Transfection with miR-766-5p inhibitor boosted LINC02418 luciferase activity, but transfection with miR-766-5p mimic decreased it. Knockdown of LINC02418 promoted miR-766-5p expression and inhibited cancer progression, which was alleviated to some extent by transfection with miR-766-5p inhibitors. Conclusion LINC02418 has the potential to serve as a poor prognostic marker for breast cancer and plays a pro-oncogenic role by targeting miR-766-5p.

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“…Additionally, they can act as scaffolds to modulate protein–protein interactions and downstream signaling pathways. Recent studies have also identified the critical role of lncRNA-mediated regulation of Wnt/β-catenin signaling in epithelial–mesenchymal transition (EMT) processes in human tumors [ 36 ]. Over the past decade or so, ncRNAs have changed their role from “junk” transcription products to functional regulatory molecules that mediate cellular processes and participate in various cellular functions in many cancers through various signaling pathways, including Wnt/β-catenin [ 37 ].…”

Section: Introduction To the Wnt Signaling Pathway And The Involvemen...mentioning

confidence: 99%

Deciphering the Enigmatic Influence: Non-Coding RNAs Orchestrating Wnt/β-Catenin Signaling Pathway in Tumor Progression

Yang,

Du,

Luo

et al. 2023

IJMS

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Dysregulated expression of specific non-coding RNAs (ncRNAs) has been strongly linked to tumorigenesis, cancer progression, and therapeutic resistance. These ncRNAs can act as either oncogenes or tumor suppressors, thereby serving as valuable diagnostic and prognostic markers. Numerous studies have implicated the participation of ncRNAs in the regulation of diverse signaling pathways, including the pivotal Wnt/β-catenin signaling pathway that is widely acknowledged for its pivotal role in embryogenesis, cellular proliferation, and tumor biology control. Recent emerging evidence has shed light on the capacity of ncRNAs to interact with key components of the Wnt/β-catenin signaling pathway, thereby modulating the expression of Wnt target genes in cancer cells. Notably, the activity of this pathway can reciprocally influence the expression levels of ncRNAs. However, comprehensive analysis investigating the specific ncRNAs associated with the Wnt/β-catenin signaling pathway and their intricate interactions in cancer remains elusive. Based on these noteworthy findings, this review aims to unravel the intricate associations between ncRNAs and the Wnt/β-catenin signaling pathway during cancer initiation, progression, and their potential implications for therapeutic interventions. Additionally, we provide a comprehensive overview of the characteristics of ncRNAs and the Wnt/β-catenin signaling pathway, accompanied by a thorough discussion of their functional roles in tumor biology. Targeting ncRNAs and molecules associated with the Wnt/β-catenin signaling pathway may emerge as a promising and effective therapeutic strategy in future cancer treatments.

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Pathological role of long non-coding (lnc) RNA in the regulation of Wnt/β-catenin signaling pathway during epithelial-mesenchymal transition (EMT)

Cited by 7 publications

References 90 publications

<i>GNAS</i> mutations suppress cell invasion by activating MEG3 in growth hormone–secreting pituitary adenoma

<i>GNAS</i> mutations suppress cell invasion by activating MEG3 in growth hormone–secreting pituitary adenoma

Expression and Significance of LINC02418 in Breast Cancer

Deciphering the Enigmatic Influence: Non-Coding RNAs Orchestrating Wnt/β-Catenin Signaling Pathway in Tumor Progression

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