Proteolipid protein 2 is associated with melanoma metastasis

Sonoda, Kotaro

doi:10.3892/or_00000645

Cited by 21 publications

(37 citation statements)

References 13 publications

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“…Experimentally passive models, which mimic the metastatic events after tumor cells enter the circulatory system by injecting tumor cells to tail veins, have been used to investigate the function of PLP2 in vivo, but the role of PLP2 in cancer cell detachment from the original site, such as adhesion to the ECM, digestion of the matrix and intravasation, has not been explored. A previous study indicated that PLP2 transfectants attach well to fibronectin, a common matrix of adhesion and migration assays (6). The present study reconfirmed those observations and showed that PLP2 or FAK miRNA may inhibit the adhesion, migration and invasion ability of B16BL6 cells in vitro.…”

Section: Discussionsupporting

confidence: 78%

“…Previous investigations have demonstrated that PLP2 associates with PI3K to activate Akt in B16F10 cells (6). Western blotting was performed for Akt phosphorylation to verify that the FAK-PI3K-Akt pathway was blocked due to suppression of PLP2 or FAK expression with the artificial miRNAs.…”

Section: Blockade Of Akt Signaling By the Plp2 Or Fak Mirnamentioning

confidence: 99%

“…Low levels of proteolipid protein 2 (PLP2) have been identified in Y925F cells by microarray analysis. Additionally, it was reported that PLP2, a four-transmembrane domain protein, has contributed to the experimental metastasis of melanoma B16F10 cells (6). Using biochemical methods, a ubiquitously expressed protein (PI3K) was identified as an associated protein of PLP2, which activates Akt, and passively enhances secretion of matrix metalloproteinase (MMP)-2 and the metastatic function of PLP2.…”

Section: Introductionmentioning

confidence: 99%

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Knockdown of proteolipid protein 2 or focal adhesion kinase with an artificial microRNA reduces growth and metastasis of B16BL6 melanoma cells

et al. 2011

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Abstract. Proteolipid protein 2 (PLP2) promotes the metastasis of B16F10 cells in an experimental metastasis model. However, the effect of PLP2 on spontaneous metastasis has yet to be demonstrated, and whether PLP2 may become a new therapeutic target for malignant tumors is as yet unknown. In this study, PLP2 or focal adhesion kinase (FAK) microRNA-based short hairpin RNAs (miRNAs) were used as target molecules to specifically reduce the expression of PLP2 or FAK in B16BL6 cells. In vitro, the knockdown of PLP2 or FAK significantly inhibited cell proliferation, adhesion, migration and invasion. In a spontaneous metastatic tumor model using a footpad injection, the knockdown of PLP2 or FAK markedly inhibited the proliferation of the primary tumor and prevented tumor cells from invading the popliteal lymph nodes. The results indicate that downregulation of PLP2 or FAK may improve outcomes of malignant tumor therapy.

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Section: Discussionsupporting

confidence: 78%

Section: Blockade Of Akt Signaling By the Plp2 Or Fak Mirnamentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Knockdown of proteolipid protein 2 or focal adhesion kinase with an artificial microRNA reduces growth and metastasis of B16BL6 melanoma cells

et al. 2011

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“…PLP2 encodes an integral membrane protein that localizes to the endoplasmic reticulum, which can multimerize and may function as an ion channel. PLP2 has been reported to be associated with melanoma metastasis [18]. PLP2 protein is necessary for downregulation of human CD99 protein in plasma membrane [19].…”

Section: Discussionmentioning

confidence: 99%

RETRACTED: miR-664 negatively regulates PLP2 and promotes cell proliferation and invasion in T-cell acute lymphoblastic leukaemia

Zhu

Miao

et al. 2015

Biochemical and Biophysical Research Communications

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“…11) In brief, 96-well flat-bottomed plates (ECM205 CytoMatrix screen kit, Chemicon, Temecula, CA, U.S.A.) coated with FN were used according to the manufacturer's protocol. A dissociation buffer was used to detach the cells from the culture plates, which were seeded at a density of 1×10 4 cells/well in 100 µL of medium and incubated at 37°C for 1 h. To remove unbound cells, the assay plates were washed with PBS.…”

mentioning

confidence: 99%

Sulfatides Inhibit Adhesion, Migration, and Invasion of Murine Melanoma B16F10 Cell Line <i>in Vitro</i>

Ozawa

Sonoda

Kato

et al. 2012

Biological & Pharmaceutical Bulletin

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Endogenous sulfatide, such as 3-sulfated galactosylceramide (3-sulfatide) has been reported to be involved in neuronal development and regulation of tumor cell metastasis. Recently, a new 6-sulfated glucosylceramide (6-sulfatide) has been isolated from the ascidian, Ciona intestinalis. To determine the antitumor function of the new sulfatide, we examined the effects of synthetic 6-sulfatide and 3-sulfatide on the metastatic features of a murine melanoma cell line, B16F10. Both sulfatides significantly inhibited the adhesion of melanoma cells onto fibronectin-coated tissue plates and, the motility and invasion of the cells, with 6-sulfatide showing stronger inhibitory activities. In addition, both sulfatides inhibited α 5 -, and β 1 -but not α v -or β 3 -integrin expression. Furthermore, these sulfatides inhibited the activation of focal adhesion kinase, Akt, and extracellular signal-regulated kinase signaling pathways, which are thought to be important for cell migration and invasion. Therefore, these sulfatides may serve as promising drug candidates for the treatment of cancer metastasis.Key words sulfatide; adhesion; motility; invasion; melanoma 3-O-Sulfogalactosylceramide (3-sulfatide), was the first sulfolipid isolated from the human brain and other tissues. 3-Sulfatide has a variety of biological functions, on the nervous system, immune system, and bacterial infection.1) It interacts with several protein, including laminin, thrombospondin, antistatin, and human immunodeficiency virus type 1 gp120.2) 3-Sulfatide on the surface of cancer cells possibly serves as a native ligand for selectin, possibly contributing to facilitation of metastasis.3,4) Thus, it has been shown that 3-sulfatide mediated carcinoma adhesion to laminin and vitronectin, modulating metastatic potential. 5,6) Further, 3LL Lewis lung carcinoma cells that highly express sulfated lactosylcceramide exhibited low adhesiveness to fibronectin (FN) and laminin. These results are attributed to the decreased expression of α 5 -, α 6 -, and β 1 integrin. 7) On the other hand, exogenous 3-sulfatide can also bind to selectin and interfere the binding of selectin to neutrophils. 8,9) Metastasis of malignant tumor cells from the primary tumor to distant sites is a complex process including adhesion, migration, invasion, and proliferation. Adhesion of melanoma cells to blood vessels may be triggered by binding selectin and their ligand. These results raised the possibility that exogenous sulfatide can suppress the metastasis. Recently, a new type of 6-sulfated glucosylceramide (6-sulfatide) was isolated from the ascidian Ciona intestinalis, but its biological function remains unknown. This finding lead us to study the biological activity, particularly the effect on the metastatic function of 6-sulfatide. In this study, we synthesized two sulfatides, 3-sulfatide (1), as an endogenous sulfatide, and a new 6-O-(sodium oxysulfonyl)-β-D-glucopyranosyl-(1 1)-(2S,3S,4R)-2-hexadecanamido-octadecane-1,3,4-triol (6-sulfatide) (2) (Fig. 1A). We examined their effec...

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Proteolipid protein 2 is associated with melanoma metastasis

Cited by 21 publications

References 13 publications

Knockdown of proteolipid protein 2 or focal adhesion kinase with an artificial microRNA reduces growth and metastasis of B16BL6 melanoma cells

Knockdown of proteolipid protein 2 or focal adhesion kinase with an artificial microRNA reduces growth and metastasis of B16BL6 melanoma cells

RETRACTED: miR-664 negatively regulates PLP2 and promotes cell proliferation and invasion in T-cell acute lymphoblastic leukaemia

Sulfatides Inhibit Adhesion, Migration, and Invasion of Murine Melanoma B16F10 Cell Line <i>in Vitro</i>

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