ArticleInternational journal of oncology2012
Relevance of amyloid precursor-like protein 2 C-terminal fragments in pancreatic cancer cells.
Article in International journal of oncology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
20 citing papers in PubMed, 29 citations in OpenAlex.
- Identification of key targets and exploration of therapeutic molecular mechanisms of natural compound tangeretin in osteosarcoma.Discover oncology · 2025Article
- Immunohistochemical profile of non-invasive follicular thyroid neoplasm with papillary-like nuclear features (NIFTP) versus other thyroid follicular lesions.Diagnostic pathology · 2025Article
- Amyloid precursor-like protein 2 expression in macrophages: differentiation and M1/M2 macrophage dynamics.Frontiers in oncology · 2025Article
- Review
- Article
- Single-cell transcriptomics reveals heterogeneity in esophageal squamous epithelial cells and constructs models for predicting patient prognosis and immunotherapy.Frontiers in immunology · 2023Article
- Research progress in the establishment of pancreatic cancer models and preclinical applications.Cancer innovation · 2022Review
- Effects of Luteolin on Human Breast Cancer Using Gene Expression Array: Inferring Novel Genes.Current issues in molecular biology · 2022Article
- The Emerging Roles of the β-Secretase BACE1 and the Long Non-coding RNA BACE1-AS in Human Diseases: A Focus on Neurodegenerative Diseases and Cancer.Frontiers in aging neuroscience · 2022Review
- Sex-dependent effects of amyloid precursor-like protein 2 in the SOD1-G37R transgenic mouse model of MND.Cellular and molecular life sciences : CMLS · 2021Article
- Molecular Characteristics of Amyloid Precursor Protein (APP) and Its Effects in Cancer.International journal of molecular sciences · 2021Review
- The emerging role of β-secretases in cancer.Journal of experimental & clinical cancer research : CR · 2021Review
- Article
- Role of APLP2 in the prognosis and clinicopathology of renal cell carcinoma.Oncology letters · 2019Article
- Beta 2-microglobulin regulates amyloid precursor-like protein 2 expression and the migration of pancreatic cancer cells.Cancer biology & therapy · 2019Article
- APLP2 Modulates JNK-Dependent Cell Migration inBioMed research international · 2018Article
- Review
- Amyloid precursor-like protein 2 (APLP2) affects the actin cytoskeleton and increases pancreatic cancer growth and metastasis.Oncotarget · 2015Article
- Amyloid precursor-like protein 2 suppresses irradiation-induced apoptosis in Ewing sarcoma cells and is elevated in immune-evasive Ewing sarcoma cells.Cancer biology & therapy · 2013Article
- Implication of Amyloid Precursor-like Protein 2 Expression in Cutaneous Squamous Cell Carcinoma Pathogenesis.In vivo (Athens, Greece)Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
In some cellular systems, particularly neurons, amyloid precursor-like protein 2 (APLP2), and its highly homologous family member amyloid precursor protein (APP), have been linked to cellular growth. APLP2 and APP undergo regulated intramembrane proteolysis to produce C-terminal fragments. In this study, we found comprehensive expression of APLP2 C-terminal fragments in a panel of pancreatic cancer cell lines; however, APP C-terminal fragments were notably limited to the BxPC3 cell line. Extensive glycosaminoglycan modification on APLP2 was also found in the majority of pancreatic cancer cell lines. Glycosaminoglycan-modified and -unmodified APLP2, and particularly APLP2 C-terminal fragments, also demonstrated increased expression in oncogene-transformed pancreatic ductal cells. Additionally, elevated APLP2 levels were confirmed in human pancreatic cancer tissue. Downregulation of APLP2 and APP expression, alone or in combination, caused a decrease in the growth of a pancreatic cancer cell line with representatively low APP C-terminal fragment expression, the S2-013 cell line. Furthermore, we found that treatment with β-secretase inhibitors to block formation of APLP2 C-terminal fragments decreased the growth and viability of S2-013 cells, without affecting the survival of a non-transformed pancreatic ductal cell line. In conclusion, our studies demonstrate that abundant APLP2, but not APP, C-terminal fragment expression is conserved in pancreatic cancer cell lines; however, APP and APLP2 equally regulated the growth of S2-013 pancreatic cancer cells. Chiefly, our discoveries establish a role for APLP2 in the growth of pancreatic cancer cells and show that inhibitors preventing APLP2 cleavage reduce the viability of pancreatic cancer cells.
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