Elevated expression of myosin VI contributes to breast cancer progression via MAPK/ERK signaling pathway

Zhan, Xi; Wang, Rui; Kuang, Xiong-Ri; Zhou, Jue-Yu; Hu, Xiaolei

doi:10.1016/j.cellsig.2023.110633

Cited by 6 publications

(4 citation statements)

References 44 publications

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“…The cell membrane channel, TRPM8, promotes tumor cell invasiveness in several cancers [47]. MYO6 upregulation drives metastasis and progression in breast, gastric, and prostate cancer [36,37,48]. The prognostic value of KRT14, TRPM8, and MYO6 in the present study suggests they may be indicative of CTC metastatic potential (Figures S5 and S12).…”

Section: Discussionmentioning

confidence: 59%

Transcriptome Profiling of Circulating Tumor Cells to Predict Clinical Outcomes in Metastatic Castration-Resistant Prostate Cancer

Groen

Kloots

Englert

et al. 2023

IJMS

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The clinical utility of circulating tumor cells (CTC) as a non-invasive multipurpose biomarker is broadly recognized. The earliest methods for enriching CTCs from whole blood rely on antibody-based positive selection. The prognostic utility of CTC enumeration using positive selection with the FDA-approved CellSearchTM system has been demonstrated in numerous studies. The capture of cells with specific protein phenotypes does not fully represent cancer heterogeneity and therefore does not realize the prognostic potential of CTC liquid biopsies. To avoid this selection bias, CTC enrichment based on size and deformability may provide better fidelity, i.e., facilitate the characterization of CTCs with any phenotype. In this study, the recently FDA-approved Parsortix® technology was used to enrich CTCs from prostate cancer (PCa) patients for transcriptome analysis using HyCEADTM technology. A tailored PCa gene panel allowed us to stratify metastatic castration-resistant prostate cancer (mCRPC) patients with clinical outcomes. In addition, our findings suggest that targeted CTC transcriptome profiling may be predictive of therapy response.

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Section: Discussionmentioning

confidence: 59%

Transcriptome Profiling of Circulating Tumor Cells to Predict Clinical Outcomes in Metastatic Castration-Resistant Prostate Cancer

Groen

Kloots

Englert

et al. 2023

IJMS

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“…Regarding potential therapeutic applications, our data also show that restoring miR-145-5p levels in prostate cancer cells, thereby reducing MYO6 levels, could be a viable strategy to suppress EMT and inhibit cell growth. Targeting MYO6 has been proposed by others as a potential therapeutic approach in gastric [63] and breast [64] cancers to suppress tumor proliferation and metastasis. A prior study revealed that concurrent overexpression of miR-145-5p and miR-143-3p, a of 20 member of the miR-145-5p family, synergistically suppressed MYO6 expression in gastric cancer, exhibiting greater inhibitory effects than miR-145-5p alone [57].…”

Section: Discussionmentioning

confidence: 99%

The Suppression of the Epithelial to Mesenchymal Transition in Prostate Cancer through the Targeting of MYO6 Using MiR-145-5p

Armstrong,

Willoughby,

McKenna

2024

IJMS

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Aberrant expression of miR-145-5p has been observed in prostate cancer where is has been suggested to play a tumor suppressor role. In other cancers, miR-145-5p acts as an inhibitor of epithelial-to-mesenchymal transition (EMT), a key molecular process for tumor progression. However, the interaction between miR-145-5p and EMT remains to be elucidated in prostate cancer. In this paper the link between miR-145-5p and EMT in prostate cancer was investigated using a combination of in silico and in vitro analyses. miR-145-5p expression was significantly lower in prostate cancer cell lines compared to normal prostate cells. Bioinformatic analysis of The Cancer Genome Atlas prostate adenocarcinoma (TCGA PRAD) data showed significant downregulation of miR-145-5p in prostate cancer, correlating with disease progression. Functional enrichment analysis significantly associated miR-145-5p and its target genes with EMT. MYO6, an EMT-associated gene, was identified and validated as a novel target of miR-145-5p in prostate cancer cells. In vitro manipulation of miR-145-5p levels significantly altered cell proliferation, clonogenicity, migration and expression of EMT-associated markers. Additional TCGA PRAD analysis suggested miR-145-5p tumor expression may be useful predictor of disease recurrence. In summary, this is the first study to report that miR-145-5p may inhibit EMT by targeting MYO6 in prostate cancer cells. The findings suggest miR-145-5p could be a useful diagnostic and prognostic biomarker for prostate cancer.

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“…It has been shown that in mice and humans, loss or point mutations within the MVI gene ( MYO6 ) lead to deafness as well as mild defects in several organs, including the brain, heart, kidney, intestines, testis, and skeletal muscles ( Avraham et al, 1997 ; Osterweil et al, 2005 ; Mohhidin et al, 2004 ; Hegan et al, 2015 ; Karatsai et al, 2023 ; Gotoh et al, 2010 ; Ameen and Apodaca 2007 ; Zakrzewski et al, 2021 ; Lehka et al, 2022 ). In addition, a significant increase in its synthesis was detected in highly malignant cancers, suggesting its important role in cell proliferation ( Yoshida et al, 2004 ; Dunn et al, 2006 ; Zhan et al, 2023 ).…”

Section: Introductionmentioning

confidence: 99%

Myosin VI in the nucleolus of neurosecretory PC12 cells: its involvement in the maintenance of nucleolar structure and ribosome organization

Nowak,

Lenartowski,

Kalita

et al. 2024

Front. Physiol.

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We have previously shown that unconventional myosin VI (MVI), a unique actin-based motor protein, shuttles between the cytoplasm and nucleus in neurosecretory PC12 cells in a stimulation-dependent manner and interacts with numerous proteins involved in nuclear processes. Among the identified potential MVI partners was nucleolin, a major nucleolar protein implicated in rRNA processing and ribosome assembly. Several other nucleolar proteins such as fibrillarin, UBF (upstream binding factor), and B23 (also termed nucleophosmin) have been shown to interact with MVI. A bioinformatics tool predicted the presence of the nucleolar localization signal (NoLS) within the MVI globular tail domain, and immunostaining confirmed the presence of MVI within the nucleolus. Depletion of MVI, previously shown to impair PC12 cell proliferation and motility, caused disorganization of the nucleolus and rough endoplasmic reticulum (rER). However, lack of MVI does not affect nucleolar transcription. In light of these data, we propose that MVI is important for nucleolar and ribosome maintenance but not for RNA polymerase 1-related transcription.

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Elevated expression of myosin VI contributes to breast cancer progression via MAPK/ERK signaling pathway

Cited by 6 publications

References 44 publications

Transcriptome Profiling of Circulating Tumor Cells to Predict Clinical Outcomes in Metastatic Castration-Resistant Prostate Cancer

Transcriptome Profiling of Circulating Tumor Cells to Predict Clinical Outcomes in Metastatic Castration-Resistant Prostate Cancer

The Suppression of the Epithelial to Mesenchymal Transition in Prostate Cancer through the Targeting of MYO6 Using MiR-145-5p

Myosin VI in the nucleolus of neurosecretory PC12 cells: its involvement in the maintenance of nucleolar structure and ribosome organization

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