Epithelial-Mesenchymal Transition (EMT) and Prostate Cancer

Odero-Marah, Valerie; Hawsawi, Ohuod; Henderson, Veronica; Sweeney, Janae D.

doi:10.1007/978-3-319-95693-0_6

Cited by 146 publications

(109 citation statements)

References 41 publications

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“…EMT is characterized by switch E-cadherin to N-cadherin and Snail, thus greatly affecting the tumor metastasis [32,33,34]. As expected, we found that the knockdown of KIFC1 increased the expression of an E-cadherin, inhibited expression levels of EMT-related transcription factors N-cadherin, Snail and ZEB1, suggesting that KIFC1 is involved in the metastasis of PTC.…”

Section: Discussionsupporting

confidence: 84%

KIFC1 accelerates the proliferation, migration and invasion of papillary thyroid cancer cells via MAPK signaling

Nie¹,

Han²,

Wen³

et al. 2020

Preprint

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Kinesin family member C1 (KIFC1) acts as a kind of minus end-directed motorized protein and is considered as an oncogene of some cancer types. However, no studies have fully elucidated its biological activity and molecular mechanisms in papillary thyroid cancer (PTC). The study focused on reporting the overexpression of KIFC1 in cell lines and tissues of PTC. Moreover, clinicopathological features analysis showed that KIFC overexpression is significantly correlated with extrathyroidal invasion and lymph node metastasis. Knockdown of KIFC1 significantly reduced cell growth, migration and invasion in PTC cells, and concomitant increased levels of differentiation markers, such as Tg and Nis. Knockdown of KIFC1 markedly increased the expression level of epithelial cell marker (E-cadherin), and decreased the expression levels of epithelial-mesenchymal transition (EMT) related transcriptional factor N-cadherin, Snail and ZEB1. Further study revealed that knockdown of KIFC1 downregulated stemness markers ALDH2 and SOX2, and inhibited the MAPK signaling cascades and downstream signaling, including p-ERK, ERK, p-JNK, JNK, MMP2, and MMP9, which can affect the expression of the EMT associated factors. Taken together, we reported that KIFC1 might promoted the proliferation, migration and invasion of PTC cells and offer a candidate molecular target for therapeutic intervention.

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Section: Discussionsupporting

confidence: 84%

KIFC1 accelerates the proliferation, migration and invasion of papillary thyroid cancer cells via MAPK signaling

Nie¹,

Han²,

Wen³

et al. 2020

Preprint

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show abstract

“…21 During PC progression, epithelial cells undergo the EMT, characterized by morphological changes in their phenotype from cuboidal to spindle-shaped. 22 Epithelial cells predominantly express E-cadherin, whereas N-cadherin is a mesenchymal protein. Vimentin, a cytoskeleton protein, has been linked to initiation of the EMT.…”

Section: Discussionmentioning

confidence: 99%

<p>MLPH Accelerates the Epithelial–Mesenchymal Transition in Prostate Cancer</p>

Zhang¹,

Sun²,

Zheng³

et al. 2020

OTT

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Introduction: Prostate cancer (PC) is the second greatest cause of cancer deaths globally. PC presents a poor prognosis once it metastasizes. There is considerable proof of vital epithelial-mesenchymal transition (EMT) functionality in PC metastasis. Previous studies revealed that melanophilin (MLPH) is associated with PC; however, its role in PC remains poorly understood. Methods: Bioinformatics analyses were performed. The cellular responses to MLPH knockdown were examined in HCC cell lines via wound healing assay, migration and invasion assay, Western blotting. Results: Analysis of the PROGgeneV2 database revealed that high MLPH expression might indicate poor overall survival. MLPH knockdown reduced PC cell migration, proliferation, and invasion. MLPH downregulation in vivo resulted in a lower growth rate and fewer metastatic nodules in lung tissues. Furthermore, MLPH knockdown recovered downregulated expression of the mesenchymal marker N-cadherin and the epithelial marker E-cadherin following a decrease in β-catenin. Conclusion: These results indicate that progression of PC is stimulated via MLPHdependent initiation of the EMT.

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“…The role of TGF-β in prostate tumors is a broad topic that has been extensively earlier reviewed [227][228][229][230], thus here we only provide a short outline of the mechanism of TGF-β actions in prostatic cancer cells.…”

Section: Prostate Cancermentioning

confidence: 99%

TGF-β and microRNA Interplay in Genitourinary Cancers

Bogusławska¹,

Kryst

Poletajew

et al. 2019

Cells

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Genitourinary cancers (GCs) include a large group of different types of tumors localizing to the kidney, bladder, prostate, testis, and penis. Despite highly divergent molecular patterns, most GCs share commonly disturbed signaling pathways that involve the activity of TGF-β (transforming growth factor beta). TGF-β is a pleiotropic cytokine that regulates key cancer-related molecular and cellular processes, including proliferation, migration, invasion, apoptosis, and chemoresistance. The understanding of the mechanisms of TGF-β actions in cancer is hindered by the “TGF-β paradox” in which early stages of cancerogenic process are suppressed by TGF-β while advanced stages are stimulated by its activity. A growing body of evidence suggests that these paradoxical TGF-β actions could result from the interplay with microRNAs: Short, non-coding RNAs that regulate gene expression by binding to target transcripts and inducing mRNA degradation or inhibition of translation. Here, we discuss the current knowledge of TGF-β signaling in GCs. Importantly, TGF-β signaling and microRNA-mediated regulation of gene expression often act in complicated feedback circuits that involve other crucial regulators of cancer progression (e.g., androgen receptor). Furthermore, recently published in vitro and in vivo studies clearly indicate that the interplay between microRNAs and the TGF-β signaling pathway offers new potential treatment options for GC patients.

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Epithelial-Mesenchymal Transition (EMT) and Prostate Cancer

Cited by 146 publications

References 41 publications

KIFC1 accelerates the proliferation, migration and invasion of papillary thyroid cancer cells via MAPK signaling

KIFC1 accelerates the proliferation, migration and invasion of papillary thyroid cancer cells via MAPK signaling

<p>MLPH Accelerates the Epithelial–Mesenchymal Transition in Prostate Cancer</p>

TGF-β and microRNA Interplay in Genitourinary Cancers

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