ArticleCarcinogenesis2014
Prolactin signaling enhances colon cancer stemness by modulating Notch signaling in a Jak2-STAT3/ERK manner.
Article in Carcinogenesis, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 80 citations in OpenAlex.
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- MiR-618 suppresses the proliferation, invasion, and migration of non-small lung cancer via the JAK2/STAT3 axis.Journal of cardiothoracic surgery · 2024Article
- Therapeutic Applications of Nanoformulated Resveratrol and Quercetin Phytochemicals in Colorectal Cancer-An Updated Review.Pharmaceutics · 2024Review
- Effects of Prolactin on Brain Neurons under Hypoxia.Life (Basel, Switzerland) · 2024Article
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- Prolactin Regulates Ovine Ovarian Granulosa Cell Apoptosis by Affecting the Expression ofInternational journal of molecular sciences · 2023Article
- JAK/STAT pathway: Extracellular signals, diseases, immunity, and therapeutic regimens.Frontiers in bioengineering and biotechnology · 2023Review
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Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Prolactin (PRL) is a secretory cytokine produced by various tissues. Binding to the cognate PRL receptor (PRLR), it activates intracellular signaling via janus kinase (JAK), extracellular signal-regulated kinase (ERK) and signal transducer and activator of transcription (STAT) proteins. PRL regulates diverse activities under normal and abnormal conditions, including malignancies. Previous clinical data suggest serum PRL levels are elevated in colorectal cancer (CRC) patients. In this study, we first determined the expression of PRL and PRLR in colon cancer tissue and cell lines. Higher levels of PRLR expression were observed in the cancer cells and cell lines compared with normal colonic epithelial cells. Incubation of colon cancer cells with PRL-induced JAK2, STAT3 and ERK1/2 phosphorylation and increased expression of Jagged 1, which is a Notch-1 receptor ligand. Notch signaling regulates CRC stem cell population. We observed increased accumulation of the cleaved/active form of Notch-1 receptor (Notch intracellular domain) and increased expression of Notch responsive genes HEY1, HES1 and stem cell marker genes DCLK1, LGR5, ALDH1 and CD44. Finally, inhibiting PRL induced JAK2-STAT3 and JAK2-ERK1/2 using AG490 and PD98059, respectively, leads to complete abrogation of Notch signaling, suggesting a role for this pathway in regulating CRC stem cells. Together, our results demonstrate that cytokine signaling induced by PRL is active in colorectal cancers and may provide a novel target for therapeutic intervention.
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