Transforming growth factor β1 signaling coincides with epithelial–mesenchymal transition and fibroblast-to-myofibroblast transdifferentiation in the development of adenomyosis in mice

Shen, Minhong; Liu, Xishi; Zhang, Hongqi; Guo, Sun‐Wei

doi:10.1093/humrep/dev314

Cited by 78 publications

(99 citation statements)

References 86 publications

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“…However, as DNA damage, oxidative stress, hypoxia, and oncogene (such as KRAS and YAP) activation induce cellular senescence and senescence would curtail fibrosis, it is likely that in older and thus more fibrotic lesions may experience less hypoxia and less oxidative stress (due to increased fibrotic content and thus reduced cellularity, less hemorrhage and thus iron overload) and less DNA damage (as seen by reduced γ‐H2AX expression ), the pressure for cellular senescence may be reduced, especially in the stromal compartment. This would be consistent with reduced Caveolin‐1 expression in adenomyosis, which can be highly fibrotic, especially as lesions get older . This also would be consistent with seemingly progressive decrease in CCN1 expression in older lesions .…”

Section: Changing Pressure For Genomic Alteration Due To Oxidative Stsupporting

confidence: 72%

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Cancer driver mutations in endometriosis: Variations on the major theme of fibrogenesis

Guo

2018

Reprod Medicine & Biology

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BackgroundOne recent study reports cancer driver mutations in deep endometriosis, but its biological/clinical significance remains unclear. Since the natural history of endometriosis is essentially gradual progression toward fibrosis, it is thus hypothesized that the six driver genes reported to be mutated in endometriosis (the RP set) may play important roles in fibrogenesis but not necessarily malignant transformation.MethodsExtensive PubMed search to see whether RP and another set of driver genes not yet reported (NR) to be mutated in endometriosis have any roles in fibrogenesis. All studies reporting on the role of fibrogenesis of the genes in both RP and NR sets were retrieved and evaluated in this review.ResultsAll six RP genes were involved in various aspects of fibrogenesis as compared with only three NR genes. These nine genes can be anchored in networks linking with their upstream and downstream genes that are known to be aberrantly expressed in endometriosis, piecing together seemingly unrelated findings.ConclusionsGiven that somatic driver mutations can and do occur frequently in physiologically normal tissues, it is argued that these mutations in endometriosis are not necessarily synonymous with malignancy or premalignancy, but the result of enormous pressure for fibrogenesis.

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Section: Changing Pressure For Genomic Alteration Due To Oxidative Stsupporting

confidence: 72%

“…Both animal and human data lend support for the notion that endometriotic lesions are fundamentally wounds undergoing repeated tissue injury and repair (ReTIAR) . Similar processes also occur in adenomyosis, due to the shared commonality of cyclic bleeding …”

Section: A Primer On the Natural History Of Endometriosismentioning

confidence: 82%

Cancer driver mutations in endometriosis: Variations on the major theme of fibrogenesis

Guo

2018

Reprod Medicine & Biology

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“…Researchers proposed a mechanism of repeated inflammatory cycle of injury and healing in adenomyotic lesions, which leads to formation of fibrotic microenvironment in myometrium. 22 Adenomyosis developmentally has a preceded timing most likely starting at early reproductive ages compared with endometrial cancers, which are mostly seen during later stages of life. Although an initial permissive myometrium is the expected microenvironment in the development of adenomyosis, eventual altered myometrial microenvironment induced by adenomyosis may cause a barrier effect and give resistance to tumor invasion.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Adenomyosis in Myometrial Invasion and Overall Survival in Endometrial Cancer

Erkılınç¹,

Taylan²,

Gülseren

et al. 2018

Int J Gynecol Cancer

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Our results showed that adenomyosis is significantly associated with lower stage in endometrial cancer that may suggest a possible limiting effect on endometrial cancer spread. In addition, despite similar rates in disease-free survival and endometrial cancer-related death, overall survival rate was significantly higher in the presence of adenomyosis and might be considered as a good prognostic factor for endometrial cancer.

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“…Epithelial‐mesenchymal transition (EMT) is one of the important mechanisms that cause early stage tumor metastasis . EMT plays a fundamental role in embryonic development and is important for organ formation and differentiation . The process of EMT involves the repression of epithelial gene expression and activation of mesenchymal gene expression .…”

Section: Introductionmentioning

confidence: 99%

Identification of new hypoxia‐regulated epithelial‐mesenchymal transition marker genes labeled by H3K4 acetylation

Wang

Yan

Wang

et al. 2019

Genes Chromosomes & Cancer

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Hypoxia‐induced epithelial‐mesenchymal transition (EMT) involves the interplay between chromatin modifiers histone deacetylase 3 (HDAC3) and WDR5. The histone mark histone 3 lysine 4 acetylation (H3K4Ac) is observed in the promoter regions of various EMT marker genes (eg, CDH1 and VIM). To further define the genome‐wide location of H3K4Ac, a chromatin immunoprecipitation followed by massively parallel DNA sequencing (ChIP‐seq) analysis was performed using a head and neck squamous cell carcinoma (HNSCC) FaDu cell line under normoxia and hypoxia. H3K4Ac was found to be located mainly around the transcription start site. Coupled with analysis of gene expression by RNA sequencing and using a HDAC3 knockdown cell line, 10 new genes (BMI1, GLI1, SMO, FOXF1, SIRT2, etc) that were labeled by H3K4Ac and regulated by HDAC3 were identified. Overexpression or knockdown of GLI1/SMO increased or repressed the in vitro migration and invasion activity in OECM‐1/FaDu cells, respectively. In HNSCC patients, coexpression of GLI1 and SMO in primary tumors correlated with metastasis. Our results identify new EMT marker genes that may play a significant role in hypoxia‐induced EMT and metastasis and further provide diagnostic and prognostic implications.

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Transforming growth factor β1 signaling coincides with epithelial–mesenchymal transition and fibroblast-to-myofibroblast transdifferentiation in the development of adenomyosis in mice

Abstract: Support for data collection and analysis was provided by grants from the National Science Foundation of China. None of the authors has anything to disclose.

Cited by 78 publications

References 86 publications

Cancer driver mutations in endometriosis: Variations on the major theme of fibrogenesis

Cancer driver mutations in endometriosis: Variations on the major theme of fibrogenesis

The Effect of Adenomyosis in Myometrial Invasion and Overall Survival in Endometrial Cancer

Identification of new hypoxia‐regulated epithelial‐mesenchymal transition marker genes labeled by H3K4 acetylation

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