Metastatic Pancreatic Adenocarcinoma Presenting as a Klatskin Tumor

Munis, Assad; Omar, Haniza; Iwaz, Suzanne; Mahdavian, Mani

doi:10.14309/02075970-201805000-00080

Cited by 1 publication

(2 citation statements)

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“…The pathogenesis of PDAC is complex and not well understood yet. Tumor metastasis has been widely observed in majority of patients with PDAC before resection due to lack of early symptoms (Munis et al 2018). Moreover, patients with PDAC may usually experience recurrence even after the surgery resection owing to the metastatic growth (Munis et al 2018).…”

Section: Introductionmentioning

confidence: 99%

“…Tumor metastasis has been widely observed in majority of patients with PDAC before resection due to lack of early symptoms (Munis et al 2018). Moreover, patients with PDAC may usually experience recurrence even after the surgery resection owing to the metastatic growth (Munis et al 2018). Therefore, investigation on the pathogenesis, development process, invasion and metastasis mechanism of PDAC could provide experimental support and theoretical basis for the early diagnosis and molecularly targeted therapy of pancreatic cancer.…”

Section: Introductionmentioning

confidence: 99%

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Desmoglein 3 contributes to tumorigenicity of pancreatic ductal adenocarcinoma through activating Src–FAK signaling

Yimamumaimaitijiang

Tuniyazi

et al. 2021

Animal Cells and Systems

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Desmogleins (DSGs), with the ability to link adjacent cells, have been shown to participate in the development of malignancy. DSG3 was up-regulated in various cancers, including lung, head and neck, and esophagus squamous cell carcinoma, which contributed to the tumor progression. The role of DSG3 in pancreatic ductal adenocarcinoma (PDAC) still remains elusive. Here, the expression of DSG3 was found to be enhanced in pancreatic cancer cell lines in vitro. Functional assays showed that shRNA-mediated knockdown of DSG3 decreased cell viability of pancreatic cancer cells and retarded the cell proliferation, migration and invasion. However, pcDNAmediated over-expression of DSG3 exhibited reversed effect on pancreatic cancer cell progression. In addition, the in vivo assay demonstrated that transfection of shDSG3 lentiviruses into pancreatic cancer cells repressed the tumorigenicity of PDAC after the cancer cells were transplanted into mice subcutaneously. Elevated DSG3 expression promoted the phosphorylation of Src (p-Src), focal adhesion kinase (p-FAK) and AKT (p-AKT) in vitro, while silence of DSG3 reduced the expression of p-Src, p-FAK and p-AKT both in vitro and in vivo. In conclusion, DSG3, as an oncogene, contributed to the tumorigenicity of PDAC through activating Src-FAK signaling.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%