S100A14 inhibits cell growth and epithelial–mesenchymal transition (EMT) in prostate cancer through FAT1-mediated Hippo signaling pathway

Jiang, Shaoqin; Zhu, Yaru; Chen, Zhenlin; Huang, Zhangcheng; Liu, Bingqiao; Xu, Yue; Li, Zhihao; Lin, Zequn; Li, Mengqiang

doi:10.1007/s13577-021-00538-8

Cited by 17 publications

(15 citation statements)

References 29 publications

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“…In particular, it is involved in the EMT processes of cell migration and invasion, which are associated with the outcome of thyroid cancer [ 41 , 42 ]. S100A14 belongs to extracellular matrix proteins that are involved in the biological process of EMT [ 20 , 43 ]. Here, we found that knockdown of S100A14 abolished ZHX2 silencing-induced cell migration both in vitro and in vivo, demonstrating that ZHX2 is involved in thyroid cancer metastasis through S100A14.…”

Section: Discussionmentioning

confidence: 99%

“…S100A14 has been reported to be dysregulated in various types of tumours and involved in the proliferation, apoptosis and signal transduction of tumour cells [ 19 ]. In particular, S100A14 regulates the epithelial-mesenchymal transition (EMT) process to influence the metastasis of prostate cancer and cervical cancer [ 20 , 21 ]. Further study clarified that S100A14 drives CCL2/CXCL5 signalling to promote breast cancer metastasis [ 22 ].…”

Section: Introductionmentioning

confidence: 99%

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ZHX2 inhibits thyroid cancer metastasis through transcriptional inhibition of S100A14

et al. 2022

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Background Thyroid cancer is the most common malignant endocrine tumour, and metastasis has become the main reason for treatment failure. However, the underlying molecular mechanism of thyroid cancer metastasis remains poorly understood. We investigated the role of the tumour suppressor zinc fingers and homeoboxes 2 (ZHX2) in the metastasis of thyroid cancer. Methods To study the role of ZHX2 in thyroid cancer metastasis, we evaluated the EMT process using cell migration, wound healing and lung metastatic tumour formation in vitro and in vivo models. Results ZHX2 expression was significantly decreased in thyroid cancer tissues, which correlated with poor prognosis of thyroid cancer patients. ZHX2 knockdown significantly promoted the migration of thyroid cancer cells. Mechanistically, ZHX2 associated with the S100 calcium binding protein A14 (S100A14) promoter to decrease the transcription of S100A14. Moreover, S100A14 was highly expressed in human thyroid cancer samples, and its expression negatively correlated with ZHX2 expression. Conclusions Inhibition of S100A14 attenuated the ZHX2 knockdown-induced enhanced metastasis of thyroid cancer cells both in vitro and in vivo. The evidence presented here suggests that ZHX2 inhibits the progression of thyroid cancer by blocking S100A14-mediated metastasis.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

ZHX2 inhibits thyroid cancer metastasis through transcriptional inhibition of S100A14

et al. 2022

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“…DIS3 was found recurrently mutated in this cohort, consistent with a recent study that described DIS3 as a predisposing gene mutated in renal MALT ( 28 , 29 ). Although described as a tumor suppressor in various cancers, FAT1 was few found mutated in lymphoma entities to date ( 30 – 32 ). Thus, we first identified potential somatic oncogenic activating mutations of FAT1 in OAML.…”

Section: Resultsmentioning

confidence: 99%

Analysis of Genetic Alterations in Ocular Adnexal Mucosa-Associated Lymphoid Tissue Lymphoma With Whole-Exome Sequencing

Zhao

Wang

et al. 2022

Front. Oncol.

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Next-generation sequencing studies on ocular adnexal marginal zone lymphoma of mucosa-associated lymphoid tissue (OAML) have to date revealed several targets of genetic aberrations. However, most of our current understanding of the pathogenesis and prognosis of OAML is primarily based on studies conducted in populations from Europe and the US. Furthermore, the majority were based on formalin-fixed paraffin-embedded (FFPE) tissue, which generally has poor integrity and creates many sequencing artifacts. To better investigate the coding genome landscapes of OAML, especially in the Chinese population, we performed whole-exome sequencing of 21 OAML cases with fresh frozen tumor tissue and matched peripheral blood samples. IGLL5, as a novel recurrently mutated gene, was found in 24% (5/21) of patients, with a higher relapse rate (P=0.032). In addition, mutations of MSH6, DIS3, FAT1, and TMEM127 were found in 10% of cases. These novel somatic mutations indicate the existence of additional/alternative lymphomagenesis pathways in OAML. Moreover, the difference between our and previous studies suggests genetic heterogeneity of OAML between Asian and Western individuals.

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“…In addition to the suppression of tumor initiation, FAT1 may also suppress metastasis. Multiple lines of evidence have suggested that inactivation of FAT1 results in epithelial-mesenchymal transition (EMT) through a variety of signaling pathways [ 28 , 30 – 33 ]. In an ESCC study, overexpression of FAT1 led to inhibition of cell proliferation and colony formation, as well as cell migration and invasion.…”

Section: Main Textmentioning

confidence: 99%

“…FAT1 knockdown led to a dramatic decrease in E-cadherin expression along with increased N-cadherin, vimentin, and snail mediated by MAPK/ERK signaling, while overexpression of FAT1 resulted in the opposite trends [ 32 ]. Jiang et alreported that S100A14 suppressed proliferation and EMT in prostate cancer [ 30 ]. It turned out that S100 calcium binding protein A14 (S100A14) promoted the expression of FAT1 and activated the Hippo complex activity, which, therefore, suppressed prostate cancer progression.…”

Section: Main Textmentioning

confidence: 99%

The diverse functions of FAT1 in cancer progression: good, bad, or ugly?

Chen

Saba

Teng

2022

J Exp Clin Cancer Res

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FAT atypical cadherin 1 (FAT1) is among the most frequently mutated genes in many types of cancer. Its highest mutation rate is found in head and neck squamous cell carcinoma (HNSCC), in which FAT1 is the second most frequently mutated gene. Thus, FAT1 has great potential to serve as a target or prognostic biomarker in cancer treatment. FAT1 encodes a member of the cadherin-like protein family. Under normal physiological conditions, FAT1 serves as a molecular “brake” on mitochondrial respiration and acts as a receptor for a signaling pathway regulating cell–cell contact interaction and planar cell polarity. In many cancers, loss of FAT1 function promotes epithelial-mesenchymal transition (EMT) and the formation of cancer initiation/stem-like cells. However, in some types of cancer, overexpression of FAT1 leads to EMT. The roles of FAT1 in cancer progression, which seems to be cancer-type specific, have not been clarified. To further study the function of FAT1 in cancers, this review summarizes recent relevant literature regarding this protein. In addition to phenotypic alterations due to FAT1 mutations, several signaling pathways and tumor immune systems known or proposed to be regulated by this protein are presented. The potential impact of detecting or targeting FAT1 mutations on cancer treatment is also prospectively discussed.

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S100A14 inhibits cell growth and epithelial–mesenchymal transition (EMT) in prostate cancer through FAT1-mediated Hippo signaling pathway

Cited by 17 publications

References 29 publications

ZHX2 inhibits thyroid cancer metastasis through transcriptional inhibition of S100A14

ZHX2 inhibits thyroid cancer metastasis through transcriptional inhibition of S100A14

Analysis of Genetic Alterations in Ocular Adnexal Mucosa-Associated Lymphoid Tissue Lymphoma With Whole-Exome Sequencing

The diverse functions of FAT1 in cancer progression: good, bad, or ugly?

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