ArticleMolecular medicine reports2014
Knockdown of OCT4 suppresses the growth and invasion of pancreatic cancer cells through inhibition of the AKT pathway.
Article in Molecular medicine reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Diagnostic significance and carcinogenic mechanism of pan-cancer gene POU5F1 in liver hepatocellular carcinoma.Cancer medicine · 2020Pooled it
- Plexin Domain Containing 2, a Protein Specifically Expressed and Elevated in Human Pancreatic Cancer Tissue and Serum, Influences Cell Proliferation by Correlating With Cortactin.Cancer medicine · 2025Article
- Multifaceted roles of OCT4 in tumor microenvironment: biology and therapeutic implications.Oncogene · 2025Review
- New insights into Notch signaling as a crucial pathway of pancreatic cancer stem cell behavior by chrysin-polylactic acid-based nanocomposite.Discover oncology · 2025Review
- Effects of growth factor deprivation on MKN-45 spheroid cells.Turkish journal of biology = Turk biyoloji dergisi · 2023Article
- OCT4 induces EMT and promotes ovarian cancer progression by regulating the PI3K/AKT/mTOR pathway.Frontiers in oncology · 2022Article
- Role of OCT4 in cancer stem-like cells and chemotherapy resistance.Biochimica et biophysica acta. Molecular basis of disease · 2020Review
- ILC3 cells promote the proliferation and invasion of pancreatic cancer cells through IL-22/AKT signaling.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2020Article
- Article
- Markers of pancreatic cancer stem cells and their clinical and therapeutic implications.Molecular biology reports · 2019Review
- Profiling of Gene Expression Associated with Stemness and Aggressiveness of ALDH1A1-Expressing Human Breast Cancer Cells.The Malaysian journal of medical sciences : MJMS · 2019Article
- Article
- Tocopherols inhibit estrogen-induced cancer stemness and OCT4 signaling in breast cancer.Carcinogenesis · 2018Article
- Clinicopathological and prognostic significance of OCT4 in patients with hepatocellular carcinoma: a meta-analysis.OncoTargets and therapy · 2018Review
- ZNF281 Promotes Growth and Invasion of Pancreatic Cancer Cells by Activating Wnt/β-Catenin Signaling.Digestive diseases and sciences · 2017Article
- eIF5A-PEAK1 Signaling Regulates YAP1/TAZ Protein Expression and Pancreatic Cancer Cell Growth.Cancer research · 2017Article
- Dual inhibiting OCT4 and AKT potently suppresses the propagation of human cancer cells.Scientific reports · 2017Article
- Article
- Concise Review: Pancreatic Cancer and Bone Marrow-Derived Stem Cells.Stem cells translational medicine · 2016Review
- The emerging roles of Oct4 in tumor-initiating cells.American journal of physiology. Cell physiology · 2015Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Octamer‑binding transcription factor 4 (OCT4) is one of the factors associated with self‑renewal and differentiation in cancer stem cells, and is crucial for the progression of various types of human malignancy. However, the expression and function of OCT4 in human pancreatic cancer has not been fully elucidated. The purpose of the present study was to investigate the function and molecular mechanisms of OCT4 in pancreatic cancer cells. The clinical significance of OCT4 expression was assessed by an immunohistochemical assay using a tissue microarray procedure in pancreatic cancer tissues and cells with different degrees of differentiation. A loss‑of‑function approach was used to examine the effects of a lentivirus‑mediated OCT4 small hairpin RNA vector on biological behaviors, including cell proliferative activity and invasive potential. The results demonstrated that the expression levels of OCT4 protein in cancer tissues were significantly elevated compared with those in adjacent non‑cancerous tissues (65.0 vs. 42.5%; P=0.005), which was correlated with tumor differentiation (P=0.008). The knockdown of OCT4 inhibited the proliferation and invasion of pancreatic cancer cells (Panc‑1) expressing high levels of OCT4, accompanied with decreased expression of AKT, proliferating cell nuclear antigen (PCNA) and matrix metalloproteinase‑2 (MMP‑2). In conclusion, the present study reveals that the increased expression of OCT4 is correlated with the differentiation of pancreatic cancer, while knockdown of OCT4 suppresses the growth and invasion of pancreatic cancer cells through inhibition of AKT pathway‑mediated PCNA and MMP‑2 expression, suggesting that OCT4 might serve as a potential therapeutic target for the treatment of pancreatic cancer.
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