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PRL-3 promotes cell adhesion by interacting with JAM2 in colon cancer

View Article: PubMed Central - PubMed

ABSTRACT

Phosphatase of regenerating liver-3 (PRL-3), also termed PTP4A3, is a metastasis-related protein tyrosine phosphatase. Its expression levels are significantly correlated with the progression and survival of a wide range of malignant tumors. However, the mechanism by which PRL-3 promotes tumor invasion and metastasis is not clear. In the present study, the functions of PRL-3 were systemically analyzed in the key events of metastasis including, motility and adhesion. A cell wounding assay, cell spread assay and cell-matrix adhesion assay were carried out to analyze the cell movement and cell adhesion ability of colon cancer, immunoprecipitation and immunofluorescence assay was confirmed the interaction of PRL-3 and JAM2. It was demonstrated that PRL-3 promoted the motility of Flp-In-293 and LoVo colon cancer cells and increased the distribution of cell skeleton proteins on the cell protrusions. In addition, stably expressing PRL-3 reduced the spreading speed of colon cancer cells and cell adhesion on uncoated, fibronectin-coated and collagen I-coated plates. Mechanistically, junction adhesion molecular 2 (JAM2) was identified as a novel interacting protein of PRL-3. The findings of the present study revealed the roles of PRL-3 in cancer cell motility and adhesion process, and provided information on the possibility of PRL-3 increase cell-cell adhesion by associating with JAM2.

No MeSH data available.


Related in: MedlinePlus

PRL3 suppresses colon cancer cell spread speed and cell-matrix adhesion. The plates were pre-coated with fibronectin or collagen I. (A) Ectopic PRL-3 reduces the cell spread speed in colon cancer cells. **P<0.05 vs. control cells. (B) Ectopic PRL-3 reduces cell-matrix adhesion. LoVo cells with stably expressed PRL-3 or control cells were seeded on the plates and the unattached cells in the indicated time points were counted. Values are expressed as the mean ± standard deviation; **P<0.05 vs. control cells.
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f2-ol-0-0-4836: PRL3 suppresses colon cancer cell spread speed and cell-matrix adhesion. The plates were pre-coated with fibronectin or collagen I. (A) Ectopic PRL-3 reduces the cell spread speed in colon cancer cells. **P<0.05 vs. control cells. (B) Ectopic PRL-3 reduces cell-matrix adhesion. LoVo cells with stably expressed PRL-3 or control cells were seeded on the plates and the unattached cells in the indicated time points were counted. Values are expressed as the mean ± standard deviation; **P<0.05 vs. control cells.

Mentions: Notably, it was observed PRL-3 reduced the spread speed of colon cancer cells (Fig. 2A). The spreading speed of control and PRL-3 transfected 293 and LoVo cells on extracellular matrix (ECM) components collagen I and fibronectin were examined 15 min after the cells were seeded. Spreading cells appeared as flattened and less refractive, whereas un-spread cells were round and brighter; the percentage of spreading cells to total cells was estimated. As presented in Fig. 2A, 293-PRL-3 and LoVo-PRL-3 cells spread much less than their respective control cells did on un-coated, collagen I-coated or fibronectin-coated plates (P<0.05). Consistently, PRL-3 expression decreased the cell-matrix adhesion in 293 and LoVo cells at the beginning time point of EDTA-digestion. The unattached cells were counted at the indicated time point following EDTA-treatment, the number of unattached cells of PRL-3 overexpressing group was dramatically higher compared to the control groups. It was concluded that PRL-3 expression promotes cell motility and actin remodeling, and PRL-3 reduces the cell spread and cell-matrix adhesion of cancer cells.


PRL-3 promotes cell adhesion by interacting with JAM2 in colon cancer
PRL3 suppresses colon cancer cell spread speed and cell-matrix adhesion. The plates were pre-coated with fibronectin or collagen I. (A) Ectopic PRL-3 reduces the cell spread speed in colon cancer cells. **P<0.05 vs. control cells. (B) Ectopic PRL-3 reduces cell-matrix adhesion. LoVo cells with stably expressed PRL-3 or control cells were seeded on the plates and the unattached cells in the indicated time points were counted. Values are expressed as the mean ± standard deviation; **P<0.05 vs. control cells.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4998106&req=5

f2-ol-0-0-4836: PRL3 suppresses colon cancer cell spread speed and cell-matrix adhesion. The plates were pre-coated with fibronectin or collagen I. (A) Ectopic PRL-3 reduces the cell spread speed in colon cancer cells. **P<0.05 vs. control cells. (B) Ectopic PRL-3 reduces cell-matrix adhesion. LoVo cells with stably expressed PRL-3 or control cells were seeded on the plates and the unattached cells in the indicated time points were counted. Values are expressed as the mean ± standard deviation; **P<0.05 vs. control cells.
Mentions: Notably, it was observed PRL-3 reduced the spread speed of colon cancer cells (Fig. 2A). The spreading speed of control and PRL-3 transfected 293 and LoVo cells on extracellular matrix (ECM) components collagen I and fibronectin were examined 15 min after the cells were seeded. Spreading cells appeared as flattened and less refractive, whereas un-spread cells were round and brighter; the percentage of spreading cells to total cells was estimated. As presented in Fig. 2A, 293-PRL-3 and LoVo-PRL-3 cells spread much less than their respective control cells did on un-coated, collagen I-coated or fibronectin-coated plates (P<0.05). Consistently, PRL-3 expression decreased the cell-matrix adhesion in 293 and LoVo cells at the beginning time point of EDTA-digestion. The unattached cells were counted at the indicated time point following EDTA-treatment, the number of unattached cells of PRL-3 overexpressing group was dramatically higher compared to the control groups. It was concluded that PRL-3 expression promotes cell motility and actin remodeling, and PRL-3 reduces the cell spread and cell-matrix adhesion of cancer cells.

View Article: PubMed Central - PubMed

ABSTRACT

Phosphatase of regenerating liver-3 (PRL-3), also termed PTP4A3, is a metastasis-related protein tyrosine phosphatase. Its expression levels are significantly correlated with the progression and survival of a wide range of malignant tumors. However, the mechanism by which PRL-3 promotes tumor invasion and metastasis is not clear. In the present study, the functions of PRL-3 were systemically analyzed in the key events of metastasis including, motility and adhesion. A cell wounding assay, cell spread assay and cell-matrix adhesion assay were carried out to analyze the cell movement and cell adhesion ability of colon cancer, immunoprecipitation and immunofluorescence assay was confirmed the interaction of PRL-3 and JAM2. It was demonstrated that PRL-3 promoted the motility of Flp-In-293 and LoVo colon cancer cells and increased the distribution of cell skeleton proteins on the cell protrusions. In addition, stably expressing PRL-3 reduced the spreading speed of colon cancer cells and cell adhesion on uncoated, fibronectin-coated and collagen I-coated plates. Mechanistically, junction adhesion molecular 2 (JAM2) was identified as a novel interacting protein of PRL-3. The findings of the present study revealed the roles of PRL-3 in cancer cell motility and adhesion process, and provided information on the possibility of PRL-3 increase cell-cell adhesion by associating with JAM2.

No MeSH data available.


Related in: MedlinePlus