2009
DOI: 10.1002/ijc.24111
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Down‐modulation of keratin 8 phosphorylation levels by PRL‐3 contributes to colorectal carcinoma progression

Abstract: Phosphatase of regenerating liver-3 (PRL-3) is a member of the PRL protein tyrosine phosphatase family and has been proposed to promote the invasiveness and metastastic capability of colorectal cancers (CRCs); however, the underlying mechanisms and target molecules of PRL-3 protein remain unknown. On the basis of the biological significance of PRL-3 phosphatase activity confirmed by the catalytically inactive PRL-3 mutant (C104S) and a PRL-3 inhibitor in CRC-derived SW480 cells, we performed protein expression… Show more

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Cited by 58 publications
(75 citation statements)
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“…One study has reported that colorectal carcinoma cells with high PRL-3 expression showed reduction or loss of phosphorylated keratin 8 expression, especially at the invasive front and in the liver metastases, indicating that it may be a metastasis suppressor [71]. In our study, we found that Keratin 8 was up-regulated after CXCR1 kockdown, which implied that CXCR1 may induce gastric tumor metastasis and invasion by reducing Keratin 8 protein.…”
Section: Discussionsupporting
confidence: 63%
“…One study has reported that colorectal carcinoma cells with high PRL-3 expression showed reduction or loss of phosphorylated keratin 8 expression, especially at the invasive front and in the liver metastases, indicating that it may be a metastasis suppressor [71]. In our study, we found that Keratin 8 was up-regulated after CXCR1 kockdown, which implied that CXCR1 may induce gastric tumor metastasis and invasion by reducing Keratin 8 protein.…”
Section: Discussionsupporting
confidence: 63%
“…27 Additionally, integrin a1, Ezrin, keratin 8 (KRT8) and CDH 22 were indentified as substrates of PRL-3. [28][29][30][31] On the other hand, the mechanisms regulating PRL-3 overexpression are not well understood. In mouse embryonic fibroblast cells with wild type but not p53 À/À , PRL-3 is induced in a p53-dependent manner.…”
Section: Discussionmentioning
confidence: 99%
“…Wang et al [23] showed that PRL-3 promoted epithelial-mesenchymal transition, leading to metastatic cancer by down-regulating PTEN via PI3K pathways. Recently, Mizuuchi et al [24] reported the direct involvement of PRL-3 in cell invasion by isolating a molecule, intermediate filament keratin 8 (KRT8), which was directly dephosphorylated by PRL-3. Therefore, PRL-3 may regulate cell invasion by modulation of phosphorylation state of known or unknown molecular targets.…”
Section: Discussionmentioning
confidence: 99%