HOXC10 promotes tumour metastasis by regulating the EMT-related gene Slug in ovarian cancer

Peng, Yuan; Li, Yuanyuan; Li, Yimin; Wu, Anqi; Fan, Lili; Huang, Wenli; Fu, Chunyan; Deng, Zhili; Wang, Kuansong; Zhang, Yu; Shu, Guang; Yin, Gang

doi:10.18632/aging.103824

Cited by 15 publications

(18 citation statements)

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“…Peng et al. confirmed that HOXC10 enhanced osteosarcoma cell metastasis by enhancing Slug transcription ( 64 ). Notably, Slug was the most important regulator of EMT in tumors ( 93 ) and was a surrogate marker of EMT in head and neck cancer ( 94 ).…”

Section: Tumor Metastasis and Invasionmentioning

confidence: 99%

“…We also provided a comprehensive description of HOXC10 expression regulation. Specifically, HOXC10 expression is regulated by several epigenetic processes, including DNA ( 6 , 50 , 96 ) and histone ( 5 , 97 ) methylation, posttranscriptional miRNA ( 10 – 12 , 59 , 61 , 64 , 98 ) and lncRNA ( 9 , 99 ) modifications, and ubiquitin modifications ( 100 ).…”

Section: Hoxc10 Expression Regulationmentioning

confidence: 99%

“…MicroRNAs (miRNAs) are small noncoding RNAs that can degrade or suppress the translation of target mRNAs by base pairing with the 3’-untranslated region (3’UTR) ( 106 ). Several miRNAs, such as miR-129-5p ( 10 – 12 ), miR-222-3p ( 64 ), miR-146b-5p ( 98 ), miRNA-221 ( 61 ), and miRNA-136 ( 59 ), have been reported to play a key role in regulating HOXC10 expression. These miRNAs directly target the 3’UTR of HOXC10 to inhibit HOXC10 expression.…”

Section: Hoxc10 Expression Regulationmentioning

confidence: 99%

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Role of HOXC10 in Cancer

Fang

Wang

et al. 2021

Front. Oncol.

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The HOXC10 gene, a member of the HOX genes family, plays crucial roles in mammalian physiological processes, such as limb morphological development, limb regeneration, and lumbar motor neuron differentiation. HOXC10 is also associated with angiogenesis, fat metabolism, and sex regulation. Additional evidence suggests that HOXC10 dysregulation is closely associated with various tumors. HOXC10 is an important transcription factor that can activate several oncogenic pathways by regulating various target molecules such as ERK, AKT, p65, and epithelial mesenchymal transition-related genes. HOXC10 also induces drug resistance in cancers by promoting the DNA repair pathway. In this review, we summarize HOXC10 gene structure and expression as well as the role of HOXC10 in different human cancer processes. This review will provide insight into the status of HOXC10 research and help identify novel targets for cancer therapy.

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Section: Tumor Metastasis and Invasionmentioning

confidence: 99%

Section: Hoxc10 Expression Regulationmentioning

confidence: 99%

Section: Hoxc10 Expression Regulationmentioning

confidence: 99%

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Role of HOXC10 in Cancer

Fang

Wang

et al. 2021

Front. Oncol.

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“…Invasion and migration are two hallmarks of the malignant biological behavior of OC, and interdiction of these progresses is a critical factor to improve biomedical treatment worldwide (22,23). EMT, a process in which stationary epithelial cells attain a highly active mesenchymal phenotype, is an essential and important step in tumor cell invasion, migration and relocalization (24)(25)(26). Downregulated expression levels of E-cadherin (a crucial epithelial marker) in epithelial cells, along with upregulated expression levels of mesenchymal proteins, including N-cadherin and slug, are common hallmarks of EMT (27,28).…”

Section: Discussionmentioning

confidence: 99%

FBXW7 inhibits invasion, migration and angiogenesis in ovarian cancer cells by suppressing VEGF expression through inactivation of β‑catenin signaling

2021

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F-box and WD repeat domain containing 7 (FBXW7) is a tumor suppressor gene frequently inactivated in several human malignancies. The present study aimed to investigate the role of FBXW7 in the invasion, migration and angiogenesis of ovarian cancer (OC) cells, and to identify its potential molecular mechanisms. First, the expression levels of FBXW7 and vascular endothelial growth factor (VEGF) were detected in several human OC cell lines using western blotting. Subsequently, FBXW7 was overexpressed to determine VEGF expression in SKOV3 cells. Transwell, wound healing and tube formation assays were performed following transfection with FBXW7 and VEGF overexpression plasmids to assess invasion, migration and angiogenesis in SKOV3 cells, respectively. Western blot analysis was performed to detect the expression levels of epithelial-to-mesenchymal transition and angiogenesis-associated proteins. In addition, the expression levels of β-catenin and c-Myc were assessed, and lithium chloride (LiCl), an agonist of β-catenin signaling, was used to elucidate the molecular mechanisms by which FBXW7 mediates its antitumor activity in OC. The results demonstrated that FBXW7 expression was markedly downregulated, whilst VEGF expression was markedly upregulated in OC cell lines compared with that in normal ovarian cells. Overexpression of FBXW7 significantly decreased VEGF expression in SKOV3 cells. Notably, overexpression of VEGF reversed the inhibitory effects of FBXW7 overexpression on the invasion, migration and angiogenesis of OC cells, accompanied by upregulated expression levels of N-cadherin, slug, CD31, VEGF receptor 1 (VEGFR1) and VEGFR2, and downregulated expression levels of E-cadherin. Furthermore, overexpression of FBXW7 markedly suppressed β-catenin and c-Myc expression, whereas the decreased expression levels of VEGF, VEGFR1 and VEGFR2 following overexpression of FBXW7 were increased after treatment of SKOV3 cells with LiCl. Overall, the results of the present study suggested that FBXW7 inhibited invasion, migration and angiogenesis of OC cells by suppressing VEGF expression through inactivation of β-catenin signaling. Thus, FBXW7 may be used as a novel therapeutic target for the treatment of OC.

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“…Moreover, in NSCLC, miR-196a antagonizes the inhibitory tumour growth effect of HOXA5, partially contributing to an increasingly invasive phenotype [109]. Another noteworthy miR target is HOXC10, shown to be involved in the EMT in both GC and ovarian OC [94,95]. Recent studies have shown that miR-136 and miR-222-3p act as an inhibitor of HOXC10, which impairs the EMT and consequently leads to less perineum and hepatic metastasis in GC and OC, respectively [94,110].…”

Section: Microrna's Interferencementioning

confidence: 99%

Roles of the HOX Proteins in Cancer Invasion and Metastasis

Paço

Garcia

Leitão-Castro

et al. 2020

Cancers

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Invasion and metastasis correspond to the foremost cause of cancer-related death, and the molecular networks behind these two processes are extremely complex and dependent on the intra- and extracellular conditions along with the prime of the premetastatic niche. Currently, several studies suggest an association between the levels of HOX genes expression and cancer cell invasion and metastasis, which favour the formation of novel tumour masses. The deregulation of HOX genes by HMGA2/TET1 signalling and the regulatory effect of noncoding RNAs generated by the HOX loci can also promote invasion and metastasis, interfering with the expression of HOX genes or other genes relevant to these processes. In this review, we present five molecular mechanisms of HOX deregulation by which the HOX clusters products may affect invasion and metastatic processes in solid tumours.

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HOXC10 promotes tumour metastasis by regulating the EMT-related gene Slug in ovarian cancer

Cited by 15 publications

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Role of HOXC10 in Cancer

Role of HOXC10 in Cancer

FBXW7 inhibits invasion, migration and angiogenesis in ovarian cancer cells by suppressing VEGF expression through inactivation of β‑catenin signaling

Roles of the HOX Proteins in Cancer Invasion and Metastasis

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