Suppression of the epithelial-mesenchymal transition by SHARP1 is linked to the NOTCH1 signaling pathway in metastasis of endometrial cancer

Liao, Yunjian; He, Xiaoyun; Qiu, Haifeng; Che, Qi; Wang, Fangyuan; Lu, Wenwen; Chen, Zheng; Qiu, Meiting; Wang, Jingyun; Wan, Xiaoping

doi:10.1186/1471-2407-14-487

Cited by 19 publications

(22 citation statements)

References 36 publications

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“…Pertinently, SHARP1 was found to play a critical role in malignant progression and acquisition of metastatic phenotypes in EC. A positive correlation was detected between SHARP1 and E-cadherin levels and negative correlation between SHARP1 and levels of JAG1, SNAIL, and vimentin (Liao et al 2014b). While a few investigators have reported downregulated expression of Notch signaling molecules (Jonusiene et al 2013, Sasnauskiene et al 2014, others found a significantly higher expression of Notch related molecules in EC as compared to normal endometrium (Mitsuhashi et al 2012).…”

Section: Cell Signaling Pathwaysmentioning

confidence: 89%

Tumor progression, metastasis, and modulators of epithelial–mesenchymal transition in endometrioid endometrial carcinoma: an update

Makker

Goel

2015

Endocrine-Related Cancer

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Endometrioid endometrial carcinoma (EEC), also known as type 1 endometrial cancer (EC), accounts for over 70-80% of all cases that are usually associated with estrogen stimulation and often develops in a background of atypical endometrial hyperplasia. The increased incidence of EC is mainly confined to this type of cancer. Most EEC patients present at an early stage and generally have a favorable prognosis; however, up to 30% of EEC present as high risk tumors, which have invaded deep into the myometrium at diagnosis and progressively lead to local or extra pelvic metastasis. The poor survival of advanced EC is related to the lack of effective therapies, which can be attributed to poor understanding of the molecular mechanisms underlying the progression of disease toward invasion and metastasis. Multiple lines of evidence illustrate that epithelial-mesenchymal transition (EMT)-like events are central to tumor progression and malignant transformation, endowing the incipient cancer cell with invasive and metastatic properties. The aim of this review is to summarize the current knowledge on molecular events associated with EMT in progression, invasion, and metastasis of EEC. Further, the role of epigenetic modifications and microRNA regulation, tumor microenvironment, and microcystic elongated and fragmented glands like invasion pattern have been discussed. We believe this article may perhaps stimulate further research in this field that may aid in identifying high risk patients within this clinically challenging patient group and also lead to the recognition of novel targets for the prevention of metastasis -the most fatal consequence of endometrial carcinogenesis.

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Section: Cell Signaling Pathwaysmentioning

confidence: 89%

Tumor progression, metastasis, and modulators of epithelial–mesenchymal transition in endometrioid endometrial carcinoma: an update

Makker

Goel

2015

Endocrine-Related Cancer

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“…[26][27][28] After validation by RT-qPCR of miRNA selected from the previous step, we found that miR-34b-5p, miR-34c-5p, miR-34c-3p, miR-375, and miR-184 emerged as being particularly relevant to determine positive or negative LN metastatic status in women with grade 1-2 early-stage EC. Furthermore, miR34b-5p, miR-34c-5p, miR-34c-3p, and miR-184 dominated the first principal component of the principal component analysis.…”

Section: Discussionmentioning

confidence: 99%

Identification of microRNA expression profile related to lymph node status in women with early-stage grade 1–2 endometrial cancer

et al. 2016

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Conventional methods used for histologic classification and grading of endometrial cancer (EC) are not sufficient to predict lymph node metastases. microRNA signatures have recently been related to EC pathologic characteristics or prognosis. The aim of this study was to evaluate whether microRNA profiles of grade 1-2 endometrioid adenocarcinomas can be related to nodal status and used as a tool to adapt surgical staging in early-stage EC. microRNA expression was assessed in nine formalin-fixed paraffin-embedded (FFPE) EC primary tumors with positive lymph node and in 27 FFPE EC primary tumors with negative lymph node, matched for grade, stage, and lymphovascular space involvement status. A microarray analysis showed that there was more than a twofold significant difference in the expression of 12 microRNAs between the two groups. A quantitative reverse transcriptase-PCR assay was used to confirm these results: the expression levels of five microRNAs (microRNA-34c-5p, -375, -184, -34c-3p, and -34b-5p) were significantly lower in the EC primary tumor with positive lymph node compared with those with negative lymph node. A minimal P-value approach revealed that women with a microRNA-375-fold change o 0.30 were more likely to have positive lymph node (n = 8; 53.3%) compared with those with a microRNA-375-fold change 40.30 (n = 1; 4.8%), P = 0.001. Furthermore, women with a microRNA 184-fold change o0.30 were more likely to have positive lymph node (n = 6; 60.0%) compared with those with a microRNA 184-fold change 40.30 (n = 3; 11.5%), P = 0.006. This is the first study investigating the relative expression of mature microRNA genes in early-stage grade 1-2 EC primary tumors according to the nodal status. This microRNA expression profile provides a potential basis for further study of the microRNA function in EC and could be used as a diagnostic tool for nodal status.

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“…SK‐N‐SH and QDDQ‐NM cells were seeded in a 24‐well plate at a density of 1 × 10 4 cells/well in 500 μL complete culture solution. When cell confluence reached 60–80%, the cells were transducted according to the lentivirus transduction manual; the purpose of the transduction was to upregulate the Beclin 1 and TRP14 genes and to establish Beclin 1 high and TRP14 high tumor cells, as previously described . The empty vector LacZ was used as a control construct.…”

Section: Methodsmentioning

confidence: 99%

“…When cell confluence reached 60-80%, the cells were transducted according to the lentivirus transduction manual; the purpose of the transduction was to upregulate the Beclin 1 and TRP14 genes and to establish Beclin 1 high and TRP14 high tumor cells, as previously described. (33) The empty vector LacZ was used as a control construct. Beclin 1 high and TRP14 high NB cells were treated with 10 nM PTX and 0.25 lmol/L SAHA.…”

Section: Methodsmentioning

confidence: 99%

Suberoylanilide hydroxamic acid sensitizes neuroblastoma to paclitaxel by inhibiting thioredoxin‐related protein 14‐mediated autophagy

Zhen¹,

Yang

et al. 2017

Cancer Science

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Paclitaxel is not as effective for neuroblastoma as most of the front‐line chemotherapeutics due to drug resistance. This study explored the regulatory mechanism of paclitaxel‐associated autophagy and potential solutions to paclitaxel resistance in neuroblastoma. The formation of autophagic vesicles was detected by scanning transmission electron microscopy and flow cytometry. The autophagy‐associated proteins were assessed by western blot. Autophagy was induced and the autophagy‐associated proteins LC3‐I, LC3‐II, Beclin 1, and thioredoxin‐related protein 14 (TRP14), were found to be upregulated in neuroblastoma cells that were exposed to paclitaxel. The inhibition of Beclin 1 or TRP14 by siRNA increased the sensitivity of the tumor cells to paclitaxel. In addition, Beclin 1‐mediated autophagy was regulated by TRP14. Furthermore, the TRP14 inhibitor suberoylanilide hydroxamic acid (SAHA) downregulated paclitaxel‐induced autophagy and enhanced the anticancer effects of paclitaxel in normal control cancer cells but not in cells with upregulated Beclin 1 and TRP14 expression. Our findings showed that paclitaxel‐induced autophagy in neuroblastoma cells was regulated by TRP14 and that SAHA could sensitize neuroblastoma cells to paclitaxel by specifically inhibiting TRP14.

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Suppression of the epithelial-mesenchymal transition by SHARP1 is linked to the NOTCH1 signaling pathway in metastasis of endometrial cancer

Cited by 19 publications

References 36 publications

Tumor progression, metastasis, and modulators of epithelial–mesenchymal transition in endometrioid endometrial carcinoma: an update

Tumor progression, metastasis, and modulators of epithelial–mesenchymal transition in endometrioid endometrial carcinoma: an update

Identification of microRNA expression profile related to lymph node status in women with early-stage grade 1–2 endometrial cancer

Suberoylanilide hydroxamic acid sensitizes neuroblastoma to paclitaxel by inhibiting thioredoxin‐related protein 14‐mediated autophagy

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