The epithelial to mesenchymal transition in pancreatic cancer: A systematic review

Beuran, Mircea; Negoi, Ionuț; Păun, Sorin; Ion, Adriana; Bleoţu, Coralia; Negoi, Ruxandra Irina; Hostiuc, Sorin

doi:10.1016/j.pan.2015.02.011

Cited by 114 publications

(89 citation statements)

References 95 publications

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“…Similarly to the majority of other carcinoma types, PC progression is associated with EMT (48). It has been widely accepted that EMT frequently occurs in PC and is involved in tumorigenesis, cancer progression and metastasis (49).…”

Section: Discussionmentioning

confidence: 99%

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Krüppel-like factor 8 induces epithelial-to-mesenchymal transition and promotes invasion of pancreatic cancer cells through transcriptional activation of four and a half LIM-only protein 2

Zai

Long

et al. 2017

Oncology Letters

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Abstract. Pancreatic cancer (PC) is one of the most aggressive types of cancer with an extremely poor prognosis. Invasive growth and early metastasis is one of the greatest challenges to overcome for the treatment of PC. Numerous previous studies have indicated that the transcription factor Krüppel-like factor 8 (KLF8) and nuclear cofactor four and a half LIM-only protein 2 (FHL2) serve important roles in tumorigenesis and tumor progression; however, their roles in PC remain elusive. The present study revealed that KLF8 and FHL2 expression is aberrantly co-overexpressed in PC tissue samples and associa ted with tumor metastasis. Furthermore, a positive correlation between the expression levels of KLF8 and FHL2 was observed. Subsequently, the present study identified KLF8 as a critical inducer of epithelial-to-mesenchymal transition (EMT) and invasion. Of note, the present study demonstrated that KLF8 overexpression induced a strong increase in FHL2 expression, and subsequent promoter reporter assays determined that KLF8 directly bound and activated the FHL2 gene promoter. Furthermore, FHL2 knockdown in KLF8-overexpressing cells partially reversed the EMT and invasive phenotypes. The present study identified KLF8-induced FHL2 activation as a novel and critical signaling mechanism underlying human PC invasion.

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Section: Discussionmentioning

confidence: 99%

“…Loss of expression of E-cadherin, an epithelial marker, is a hallmark of EMT (6,48,50). An increasing number of transcription factors have been implicated in the repression of E-cadherin expression, including KLF transcription factor family proteins (6,23).…”

Section: Discussionmentioning

confidence: 99%

Krüppel-like factor 8 induces epithelial-to-mesenchymal transition and promotes invasion of pancreatic cancer cells through transcriptional activation of four and a half LIM-only protein 2

Zai

Long

et al. 2017

Oncology Letters

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“…Regarding the upregulation of EMT markers, previously it has been described that chemoresistance to doxorubicin induces EMT in colon cancer and lung cancer cells [37,38]. Furthermore, in several tumor types, including pancreatic adenocarcinoma (PDAC), a link has been described between CSCs and EMT [39]. Although it is difficult to determine which event occurs first, a likely explanation is that EMT contributes to the establishment of CSCs.…”

Section: Discussionmentioning

confidence: 99%

Identification of CD90 as Putative Cancer Stem Cell Marker and Therapeutic Target in Insulinomas

Buishand

Arkesteijn

Feenstra

et al. 2016

Stem Cells and Development

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The long-term prognosis after surgical resection of malignant insulinoma (INS) is poor. Novel adjuvant therapies, specifically targeting cancer stem cells (CSCs), are warranted. Therefore, the goal of this study was to characterize and target putative INS CSCs. Using fluorescence-activated cell sorting, human INS cell line CM and pancreatic carcinoid cell line BON1 were screened for the presence of stem cell-associated markers. CD90, CD166, and GD2 were identified as potential CSC markers. Only CD90 + INS cells had an increased tumor-initiating potential in athymic nude mice. Anti-CD90 monoclonal antibodies decreased the viability and metastatic potential of injected cells in a zebrafish embryo INS xenograft model. Primary INS stained positive for CD90 by immunohistochemistry, however also intratumoral fibroblasts and vascular endothelium showed positive staining. The results of this study suggest that anti-CD90 monoclonals form a potential novel adjuvant therapeutic modality by targeting either INS cells directly, or by targeting the INS microenvironment.

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“…E-cadherin, together with associated catenins, plays a key role in maintaining cell-cell adhesion, but which are lost or disturbed in cancer cells, mainly due to the loss of E-cadherin in cancer cells. Hence, reduced cell-cell adhesion after down-regulation of E-cadherin enhances the potential for metastatic dissemination of cancer cells (Beuran et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

Suppression of the Epidermal Growth Factor-like Domain 7 and Inhibition of Migration and Epithelial-Mesenchymal Transition in Human Pancreatic Cancer PANC-1 Cells

Wang

Dong

Yang³

et al. 2015

Asian Pacific Journal of Cancer Prevention

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The epithelial to mesenchymal transition in pancreatic cancer: A systematic review

Cited by 114 publications

References 95 publications

Krüppel-like factor 8 induces epithelial-to-mesenchymal transition and promotes invasion of pancreatic cancer cells through transcriptional activation of four and a half LIM-only protein 2

Krüppel-like factor 8 induces epithelial-to-mesenchymal transition and promotes invasion of pancreatic cancer cells through transcriptional activation of four and a half LIM-only protein 2

Identification of CD90 as Putative Cancer Stem Cell Marker and Therapeutic Target in Insulinomas

Suppression of the Epidermal Growth Factor-like Domain 7 and Inhibition of Migration and Epithelial-Mesenchymal Transition in Human Pancreatic Cancer PANC-1 Cells

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