MMI-166 is a third-generation selective matrix metalloproteinase (MMP) inhibitor that prevents tumor invasion and metastasis by downregulating the activity of MMP-2 and MMP-9. However, MMI-166's effect in pancreatic cancer cells has not been widely studied. Initially, we treated SW1990, human pancreatic cancer cells, with 0, 50 or 100 μg/ml of MMI-166 for 24 h. Apoptosis in the cells was then observed by inverted fluorescence microscope and flow cytometry; the apoptosis rate was dependent on MMI-166 concentration. We then injected nude mice with SW1990 cells. Volume of the resulting xenograft tumors in nude mice treated with MMI-166 was far less than that of the control group, whereas their apoptotic index was much greater. Expression of MMP-2, MMP-9, c-myc and survivin were markedly lower in tumors from the treated mice than in the control group. In cell experiments, MMP-2 and MMP-9 activities were downregulated by MMI-166 compared with controls, as were both mRNA and protein levels of MMP-2, MMP-9 and c-myc, although survivin expression did not differ. These results show that MMI-166 can induce apoptosis of pancreatic cancer cells in vitro and in vivo. The mechanism may be related to downregulation of c-myc by MMI-166.
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http://dx.doi.org/10.1007/s12032-014-0418-5 | DOI Listing |
Cancer Cytopathol
February 2025
Department of Pathology, Massachusetts General Hospital, Boston, Massachusetts, USA.
Background: Major mutations (e.g., KRAS, GNAS, TP53, SMAD4) in pancreatic cyst fluid (PCF) are useful for classifying and risk stratifying certain cyst types, particularly in cases with nondiagnostic cytology.
View Article and Find Full Text PDFUnited European Gastroenterol J
January 2025
"Carol Davila" University of Medicine and Pharmacy, Bucharest, Romania.
The rising incidence of pancreatic diseases, including acute and chronic pancreatitis and various pancreatic neoplasms, poses a significant global health challenge. Pancreatic ductal adenocarcinoma (PDAC) for example, has a high mortality rate due to late-stage diagnosis and its inaccessible location. Advances in imaging technologies, though improving diagnostic capabilities, still necessitate biopsy confirmation.
View Article and Find Full Text PDFJ Exp Clin Cancer Res
January 2025
Department of Hepato-Biliary-Pancreatic Surgery, General Surgery, Huadong Hospital, Fudan University, Shanghai, 200040, PR China.
Purpose: Glucose starvation induces the accumulation of disulfides and F-actin collapse in cells with high expression of SLC7A11, a phenomenon termed disulfidptosis. This study aimed to confirm the existence of disulfidptosis in pancreatic ductal adenocarcinoma (PDAC) and elucidate the role of Cancer Susceptibility 8 (CASC8) in this process.
Methods: The existence of disulfidptosis in PDAC was assessed using flow cytometry and F-actin staining.
Sci Rep
January 2025
State Key Laboratory of Holistic Integrative Management of Gastrointestinal Cancers, Beijing Key Laboratory of Carcinogenesis and Translational Research, Department of Pathology, Peking University Cancer Hospital and Institute, 52 Fucheng Road, Haidian District, Beijing, 100142, China.
Delta-like protein (DLL3) is a novel therapeutic target. DLL3 expression in gastroenteropancreatic neuroendocrine tumors (GEP-NECs) is poorly understood, complicating the distinction between well-differentiated neuroendocrine tumors G3 (NET G3) and poorly differentiated NEC. DLL3 immunohistochemistry (IHC) was performed on 248 primary GEP-NECs, correlating with clinicopathological parameters, NE markers, PD-L1, Ki67 index, and prognosis.
View Article and Find Full Text PDFSurgery
January 2025
Division of Surgical Oncology, Lehigh Valley Topper Cancer Institute, Allentown, PA. Electronic address:
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