Suppression of the proliferation and invasion of breast cancer cells by <scp>ST</scp>7L occurs through inhibition of activation of Wnt/<scp>GSK</scp>‐3β/β‐catenin signalling

Wang, Hua; Sun, Lei; Jiang, Jue; Yu, Shanshan; Zhou, Qi

doi:10.1111/1440-1681.13166

Cited by 8 publications

(4 citation statements)

References 21 publications

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“…So far, no previous studies showed either of these genes to be related to bladder cancer risk. As ST7L is a key factor of Wnt/GSK-3β/β-catenin signaling pathway, 46,47 the interaction with ADSS2 might inhibit the function of ST7L that is the suppression of tumorigenicity, and thereby enhance the development of bladder cancer. Similarly, the LARP4B (10:890252)-LHPP (10:126164319) interaction was also found to increase the bladder cancer risk in both Caucasian and non-Caucasian participants.…”

Section: Discussionmentioning

confidence: 99%

Genome‐wide exploration of genetic interactions for bladder cancer risk

Yu,

Tang,

Chen

et al. 2023

Intl Journal of Cancer

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Although GWASs have been conducted to investigate genetic variation of bladder tumorigenesis, little is known about genetic interactions that may influence bladder cancer (BC) risk. By leveraging large‐scale participants from UK Biobank, we established a discovery database with 4000 Caucasian participants (2000 cases vs 2000 non‐cases), a database with 1648 Caucasian participants (824 cases vs 824 non‐cases) and 856 non‐Caucasian participants (428 cases vs 428 non‐cases) as validation. We then performed a genome‐wide SNP‐SNP interaction investigation related to BC risk based a machine learning approach (ie, GenEpi). Moreover, we used the selected interactions to build a BC screening model with an integrated interaction‐empowered polygenic risk score (iPRS) based on Cox proportional hazard model. With Bonferroni correction, we identified 10 statistically significant pairs of SNPs, which located in 17 chromosomes. Of these, four SNP‐SNP interactions were found to be positively associated with BC risk among Caucasian participants (ORs 1.57‐2.03), while six SNP‐SNP interactions showed negatively associated with BC risk (ORs 0.54‐0.65). Only four of the SNP‐SNP interactions were consistently identified in non‐Caucasian participants located in ST7L‐ADSS2, FHIT‐CHDH, LARP4B‐LHPP and RBFOX3‐MPRIP. In addition, the iPRS showed a HR of 1.81 (95% CI: 1.46‐2.09) compared the highest tertile to the lowest tertile, with an enhanced AUC (0.91; 95% CI:0.85‐0.97) than PRS (AUC: 0.86; 95% CI:0.76‐0.95; P‐DeLong test = 2.2 × 10−4). In summary, this study identified several important SNP‐SNP interactions for BC risk, and developed an iPRS model for BC screening, which may help to identify the people at high‐risk state of BC before early manifestation.

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Section: Discussionmentioning

confidence: 99%

Genome‐wide exploration of genetic interactions for bladder cancer risk

Yu,

Tang,

Chen

et al. 2023

Intl Journal of Cancer

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“…It reduces the expression level of β-catenin and GSK-3β phosphorylation, leading to inhibition of β-catenin transcription. Consequently, knockdown of ST7L promotes growth, invasion, and EMT of tumor cells [ 175 ]. There was miR-331-3p up regulations in PC cells and clinical specimens, which was associated with the advanced stage and distant invasion.…”

Section: Wnt Signaling Pathwaymentioning

confidence: 99%

MicroRNAs as the critical regulators of epithelial mesenchymal transition in pancreatic tumor cells

Tolue Ghasaban,

Ghanei,

Mahmoudian

et al. 2024

Heliyon

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“…Wang et al [ 34 ] first demonstrated that the expression of the suppression of tumorigenicity 7 like ( ST7L ) is downregulated in BC cells, and more importantly, that ST7L acts as an antitumor supervisor by reducing GSK-3β phosphorylation and inducing β-catenin degradation. However, the mechanisms through which ST7L controls GSK-3β phosphorylation are still missing ( Table 1 ).…”

Section: Canonical Wnt Pathway and Bcmentioning

confidence: 99%

The Wnt Signalling Pathway: A Tailored Target in Cancer

Koni

Pinnarò

Brizzi

2020

IJMS

115

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Cancer is one of the greatest public health challenges. According to the World Health Organization (WHO), 9.6 million cancer deaths have been reported in 2018. The most common cancers include lung, breast, colorectal, prostate, skin (non-melanoma) and stomach cancer. The unbalance of physiological signalling pathways due to the acquisition of mutations in tumour cells is considered the most common cancer driver. The Wingless-related integration site (Wnt)/β-catenin pathway is crucial for tissue development and homeostasis in all animal species and its dysregulation is one of the most relevant events linked to cancer development and dissemination. The canonical and the non-canonical Wnt/β-catenin pathways are known to control both physiological and pathological processes, including cancer. Herein, the impact of the Wnt/β-catenin cascade in driving cancers from different origin has been examined. Finally, based on the impact of Extracellular Vesicles (EVs) on tumour growth, invasion and chemoresistance, and their role as tumour diagnostic and prognostic tools, an overview of the current knowledge linking EVs to the Wnt/β-catenin pathway is also discussed.

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Suppression of the proliferation and invasion of breast cancer cells by ST7L occurs through inhibition of activation of Wnt/GSK‐3β/β‐catenin signalling

Cited by 8 publications

References 21 publications

Genome‐wide exploration of genetic interactions for bladder cancer risk

Genome‐wide exploration of genetic interactions for bladder cancer risk

MicroRNAs as the critical regulators of epithelial mesenchymal transition in pancreatic tumor cells

The Wnt Signalling Pathway: A Tailored Target in Cancer

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