ArticleExperimental cell research2011
Ligand stimulation of ErbB4 and a constitutively-active ErbB4 mutant result in different biological responses in human pancreatic tumor cell lines.
Article in Experimental cell research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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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Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
- Does the ERBB/EGF Signaling Network Serve as a Nexus for Oncogenic Signals in Uveal Melanoma?Biomolecules · 2026Review
- The Yin and Yang of ERBB4: Tumor Suppressor and Oncoprotein.Pharmacological reviews · 2022Review
- A Review of HER4 (ErbB4) Kinase, Its Impact on Cancer, and Its Inhibitors.Molecules (Basel, Switzerland) · 2021Review
- Unraveling ERBB network dynamics upon betacellulin signaling in pancreatic ductal adenocarcinoma in mice.Molecular oncology · 2020Article
- The role of ErbB4 in cancer.Cellular oncology (Dordrecht, Netherlands) · 2020Review
- The protective effect of betacellulin against acute pancreatitis is ERBB4 dependent.Journal of gastroenterology · 2020Article
- Combating pancreatic cancer with PI3K pathway inhibitors in the era of personalised medicine.Gut · 2019Review
- Mig-6 deficiency cooperates with oncogenic Kras to promote mouse lung tumorigenesis.Lung cancer (Amsterdam, Netherlands) · 2017Article
- ERBB4 Expression in Ovarian Serous Carcinoma Resistant to Platinum-Based Therapy.Cancer control : journal of the Moffitt Cancer Center · 2017Article
- Deregulation of the EGFR/PI3K/PTEN/Akt/mTORC1 pathway in breast cancer: possibilities for therapeutic intervention.Oncotarget · 2014Review
- Multiple Functional Motifs Are Required for the Tumor Suppressor Activity of a Constitutively-Active ErbB4 Mutant.Journal of cancer research and therapeutic oncology · 2013Article
- The absence of the ERBB4 hotspot mutations in melanomas in patients from southern China.Chinese journal of cancer · 2013Article
- Directing HER4 mRNA expression towards the CYT2 isoform by antisense oligonucleotide decreases growth of breast cancer cells in vitro and in vivo.British journal of cancer · 2013Article
- Slow down to stay alive: HER4 protects against cellular stress and confers chemoresistance in neuroblastoma.Cancer · 2012Article
- EGFR ligands exhibit functional differences in models of paracrine and autocrine signaling.Growth factors (Chur, Switzerland) · 2012Review
- The Q43L mutant of neuregulin 2β is a pan-ErbB receptor antagonist.The Biochemical journal · 2012Article
- Article
- ErbB2 Is Necessary for ErbB4 Ligands to Stimulate Oncogenic Activities in Models of Human Breast Cancer.Genes & cancer · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Pancreatic cancer is the fourth leading cause of cancer death in the United States. Indeed, it has been estimated that 37,000 Americans will die from this disease in 2010. Late diagnosis, chemoresistance, and radioresistance of these tumors are major reasons for poor patient outcome, spurring the search for pancreatic cancer early diagnostic and therapeutic targets. ErbB4 (HER4) is a member of the ErbB family of receptor tyrosine kinases (RTKs), a family that also includes the Epidermal Growth Factor Receptor (EGFR/ErbB1/HER1), Neu/ErbB2/HER2, and ErbB3/HER3. These RTKs play central roles in many human malignancies by regulating cell proliferation, survival, differentiation, invasiveness, motility, and apoptosis. In this report we demonstrate that human pancreatic tumor cell lines exhibit minimal ErbB4 expression; in contrast, these cell lines exhibit varied and in some cases abundant expression and basal tyrosine phosphorylation of EGFR, ErbB2, and ErbB3. Expression of a constitutively-dimerized and -active ErbB4 mutant inhibits clonogenic proliferation of CaPan-1, HPAC, MIA PaCa-2, and PANC-1 pancreatic tumor cell lines. In contrast, expression of wild-type ErbB4 in pancreatic tumor cell lines potentiates stimulation of anchorage-independent colony formation by the ErbB4 ligand Neuregulin 1β. These results illustrate the multiple roles that ErbB4 may be playing in pancreatic tumorigenesis and tumor progression.
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