Background/aims: The cell surface protein transmembrane 4 L6 family member 1 (TM4SF1) has been detected in various tumors and plays a major role in the development of cancer. We aimed to investigate the effects of TM4SF1 on the migration and invasion of pancreatic cancer in vitro and in vivo and explore its related molecular mechanisms.
Methods: qRT-PCR and immunohistochemical analyses were used to measure the expression of TM4SF1 in pancreatic cancer tissues and adjacent tissues. TM4SF1 was silenced using siRNA and shRNA to investigate the role of this protein in the proliferation and metastasis of pancreatic cancer cells. MTS and Transwell assays were used to examine the effect of TM4SF1 on pancreatic cancer cell lines. The expression and activity of MMP-2 and MMP-9 were determined by qRT-PCR, western blots and gelatin zymography. In vivo, orthotopic pancreatic tumor models were used to examine the formation of metastasis.
Results: qRT-PCR and immunohistochemical analyses showed that TM4SF1 was highly expressed in pancreatic cancer tissues compared with the adjacent tissues. In in vitro experiments the silencing of TM4SF1 reduced cell migration and invasion and down-regulated the expression and activity of MMP-2 and MMP-9. However, no significant difference in cell proliferation was detected after silencing TM4SF1. Additionally, knocking down TM4SF1 decreased the formation of lung and liver metastases in orthotopic pancreatic tumor models.
Conclusion: Our results demonstrate that the expression of TM4SF1 is higher in pancreatic cancer tissues and pancreatic cancer cell lines than controls. Knockdown of TM4SF1 inhibited the migration and invasion of pancreatic cancer cells by regulating the expression and activity of MMP-2 and MMP-9, which suggests that TM4SF1 may play a significant role in metastasis in pancreatic cancer.
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http://dx.doi.org/10.1159/000445664 | 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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