Ras‑Related Protein Rab‑38 (RAB38), which belongs to the RAB family, is involved in the biogenesis of lysosome‑related organelles and defense against certain microbial infections. However, the clinical significance and potential function of RAB38 in pancreatic adenocarcinoma remain unclear. In the present study, an immunohistochemical assay was performed to analyze the expression of RAB38 in pancreatic adenocarcinoma tumor specimens from 82 patients, and the clinicopathological characteristics and survival rate of these patients were further examined. To validate the role of RAB38 in tumors, the effect of RAB38 on tumor cell proliferation, migration and invasion was assessed by establishing RAB38 knockdown cell lines. Reverse transcription‑quantitative polymerase chain reaction and western blotting were used to examine the expression levels of proteins associated with the cancer cell behavior. In addition, the inhibitory effect of RAB38 silencing on pancreatic cancer was examined in mice. The immunohistochemistry results revealed that RAB38 was upregulated and positively correlated with the grade of progression in pancreatic adenocarcinoma patients. Further investigation indicated that RAB38 downregulation significantly suppressed the proliferation, migration and invasive capacity of pancreatic cancer cells, as well as decreased the expression levels of Ki67, proliferating cell nuclear antigen, and matrix metalloproteinases 2 and 9. RAB38 silencing also inhibited the development of pancreatic cancer in vivo. Taken together, a high level of RAB38 was significantly associated with the malignant phenotypes of pancreatic cancer, suggesting that RAB38 may serve as a novel biomarker and a potential therapeutic target for pancreatic cancer.
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http://dx.doi.org/10.3892/mmr.2018.9732 | DOI Listing |
Ann Med
December 2025
Department of Surgery, Faculty of Medicine, Unit of Hepato-Pancreato-Biliary Surgery and Abdominal Organ Transplantation, Doce de Octubre University Hospital, Instituto de Investigación (imas12), Complutense University, Madrid, Spain.
Background: Delayed gastric emptying (DGE) is a frequent complication of pancreatoduodenectomy (PD) and is associated with prolonged hospital stay, readmission, increased hospital costs and decreased quality of life. However, the pathophysiology of DGE remains unclear.
Methods: This is a retrospective study of patients who underwent PD for pancreatic or periampullary tumours.
Phys Imaging Radiat Oncol
January 2025
Department of Radiation Oncology, Hokkaido University Faculty of Medicine and Graduate School of Medicine, North 15 West 7, Kita-ku, Sapporo, Hokkaido 060-8638, Japan.
Background And Purpose: Radiation-induced lymphopenia (RIL) may be associated with a worse prognosis in pancreatic cancer. This study aimed to develop a normal tissue complication probability (NTCP) model to predict severe RIL in patients with pancreatic cancer undergoing concurrent chemoradiotherapy (CCRT).
Materials And Methods: We reviewed pancreatic cancer patients treated at our facility for model training and internal validation.
Ann Transl Med
December 2024
Institute for Tumor Immunology, Center for Tumor Biology and Immunology, Philipps-University Marburg, Marburg, Germany.
One of the most important targets for natural killer (NK) cell-mediated therapy is the induction of natural killer group 2D ligand (NKG2D-L) expression. APTO253 is a small molecule that selectively kills acute myeloid leukemia (AML) cells, and it has been reported that APTO253 can induce Krüppel-like factor 4 (KLF4) expression and downregulate c-MYC expression. Recently, we discovered a novel role of APTO253 in modulating the NK cell response by inducing surface expression of NKG2D-Ls, especially MHC class I polypeptide-related sequence A (MICA), in AML cells.
View Article and Find Full Text PDFAnn Transl Med
December 2024
Department of Clinical Oncology, The Christie NHS Foundation Trust, Manchester, UK.
World J Gastrointest Oncol
January 2025
Faculty of Medicine, Carol Davila University of Medicine and Pharmacy, Bucharest 050474, Romania.
Background: Pancreatic ductal adenocarcinoma (PDAC) is an aggressive lethal malignancy with limited options for treatment and a 5-year survival rate of 11% in the United States. As for other types of tumors, such as colorectal cancer, aberrant lipid synthesis and reprogrammed lipid metabolism have been suggested to be associated with PDAC development and progression.
Aim: To identify the possible involvement of lipid metabolism in PDAC by analyzing in tumoral and non-tumoral tissues the expression level of the most relevant genes involved in the long-chain fatty acid (FA) import into cell.
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