ArticleMolecular cancer research : MCR2011
Cross-talk between phospho-STAT3 and PLCγ1 plays a critical role in colorectal tumorigenesis.
Article in Molecular cancer research : MCR, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 34 citations in OpenAlex.
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- Emerging Role of Plant-Based Dietary Components in Post-Translational Modifications Associated with Colorectal Cancer.Life (Basel, Switzerland) · 2023Review
- Simultaneous augmentation of muscle and bone by locomomimetism through calcium-PGC-1α signaling.Bone research · 2022Article
- GVES: machine learning model for identification of prognostic genes with a small dataset.Scientific reports · 2021Article
- Long non‑coding RNA SNHG20 promotes colorectal cancer cell proliferation, migration and invasion via miR‑495/STAT3 axis.Molecular medicine reports · 2021Article
- Phosphoinositide-Dependent Signaling in Cancer: A Focus on Phospholipase C Isozymes.International journal of molecular sciences · 2020Review
- STAT3 Activation and Oncogenesis in Lymphoma.Cancers · 2019Review
- Phospholipase Cγ1 links inflammation and tumorigenesis in colitis-associated cancer.Oncotarget · 2018Article
- Peptide microarray profiling identifies phospholipase C gamma 1 (PLC-γ1) as a potential target for t(8;21) AML.Oncotarget · 2017Article
- Article
- Lentivirus-mediated PLCγ1 gene short-hairpin RNA suppresses tumor growth and metastasis of human gastric adenocarcinoma.Oncotarget · 2016Article
- WISP-2 in human gastric cancer and its potential metastatic suppressor role in gastric cancer cells mediated by JNK and PLC-γ pathways.British journal of cancer · 2015Article
- Rhomboid domain containing 1 promotes colorectal cancer growth through activation of the EGFR signalling pathway.Nature communications · 2015Article
- Review
- LPA Induces Colon Cancer Cell Proliferation through a Cooperation between the ROCK and STAT-3 Pathways.PloS one · 2015Article
- HDAC8 and STAT3 repress BMF gene activity in colon cancer cells.Cell death & disease · 2014Article
- Novel carbazole inhibits phospho-STAT3 through induction of protein-tyrosine phosphatase PTPN6.Journal of medicinal chemistry · 2014Article
- Ube2g2-gp78-mediated HERP polyubiquitylation is involved in ER stress recovery.Journal of cell science · 2014Article
- Gain of interaction with IRS1 by p110α-helical domain mutants is crucial for their oncogenic functions.Cancer cell · 2013Article
- Identification and functional characterization of p130Cas as a substrate of protein tyrosine phosphatase nonreceptor 14.Oncogene · 2013Article
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
Hyperphosphorylation at the Y705 residue of signal transducer and activator of transcription 3 (STAT3) is implicated in tumorigenesis of leukemia and some solid tumors. However, its role in the development of colorectal cancer is not well defined. To rigorously test the impact of this phosphorylation on colorectal tumorigenesis, we engineered a STAT3 Y705F knock-in to interrupt STAT3 activity in HCT116 and RKO colorectal cancer cells. These STAT3 Y705F mutant cells fail to respond to cytokine stimulation and grow slower than parental cells. These mutant cells are also greatly diminished in their abilities to form colonies in culture, to exhibit anchorage-independent growth in soft agar, and to grow as xenografts in nude mice. These observations strongly support the premise that STAT3 Y705 phosphorylation is crucial in colorectal tumorigenesis. Although it is generally believed that STAT3 functions as a transcription factor, recent studies indicate that transcription-independent functions of STAT3 also play an important role in tumorigenesis. We show here that wild-type STAT3, but not STAT3 Y705F mutant protein, associates with phospholipase Cγ1 (PLCγ1). PLCγ1 is a central signal transducer of growth factor and cytokine signaling pathways that are involved in tumorigenesis. In STAT3 Y705F mutant colorectal cancer cells, PLCγ1 activity is reduced. Moreover, overexpression of a constitutively active form of PLCγ1 rescues the transformation defect of STAT3 Y705F mutant cells. In aggregate, our study identifies previously unknown cross-talk between STAT3 and the PLCγ signaling pathways that may play a critical role in colorectal tumorigenesis.
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