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L1cam promotes tumor progression and metastasis and is an independent unfavorable prognostic factor in gastric cancer.

Chen DL, Zeng ZL, Yang J, Ren C, Wang DS, Wu WJ, Xu RH - J Hematol Oncol (2013)

Bottom Line: Previous reports have demonstrated that L1cam is aberrantly expressed in various tumors.Ectopic expression of L1cam in gastric cell lines significantly promoted cell proliferation, migration and invasion whereas knockdown of L1cam inhibited cell proliferation, migration and invasion in vitro as well as tumorigenesis and metastasis in vivo.The low level of phosphorylated Akt in HGC27 cells was up-regulated after ectopic expression of L1cam, whereas the high level of phosphorylated Akt in SGC7901 cells was suppressed by knockdown of L1cam.

View Article: PubMed Central - HTML - PubMed

Affiliation: State Key Laboratory of Oncology in South China, Sun Yat-sen University Cancer Center, 651 Dong Feng East Load, Guangzhou 510060, China.

ABSTRACT

Background: Previous reports have demonstrated that L1cam is aberrantly expressed in various tumors. The potential role of L1cam in the progression and metastasis of gastric cancer is still not clear and needs exploring.

Methods: Expression of L1cam was evaluated in gastric cancer tissues and cell lines by immunohistochemistry and Western blot. The relationship between L1cam expression and clinicopathological characteristics was analyzed. The effects of L1cam on cell proliferation, migration and invasion were investigated in gastric cancer cell lines both in vitro and in vivo. The impact of L1cam on PI3K/Akt pathway was also evaluated.

Results: L1cam was overexpressed in gastric cancer tissues and cell lines. L1cam expression was correlated with aggressive tumor phenotype and poor overall survival in gastric cancer patients. Ectopic expression of L1cam in gastric cell lines significantly promoted cell proliferation, migration and invasion whereas knockdown of L1cam inhibited cell proliferation, migration and invasion in vitro as well as tumorigenesis and metastasis in vivo. The low level of phosphorylated Akt in HGC27 cells was up-regulated after ectopic expression of L1cam, whereas the high level of phosphorylated Akt in SGC7901 cells was suppressed by knockdown of L1cam. Moreover, the migration and invasion promoted by L1cam overexpression in gastric cancer cells could be abolished by either application of LY294002 (a phosphoinositide-3-kinase inhibitor) or knockdown of endogenous Akt by small interfering RNA.

Conclusions: Our study demonstrated that L1cam, overexpressed in gastric cancer and associated with poor prognosis, plays an important role in the progression and metastasis of gastric cancer.

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Related in: MedlinePlus

L1cam affects the reponsiveness to oxaliplatin of gastric cancer cells. (A) SGC7901 cells were transfected with sh-L1cam or sramble lentivirus. Cells were left untreated or administrated with different concentrations of oxaliplatin and cell cycle analyses were performed. Graph indicates the percentage of cells in sub G1/G0 phase (apoptotic cells), *P <0.05. (B) HGC27 cells were transfected with L1cam or negative control vectors. Cells were left untreated or administrated with different concentrations of oxaliplatin and cell cycle analyses were performed. Graph indicates the percentage of cells in sub G1/G0 phase (apoptotic cells), *P <0.05.
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Figure 4: L1cam affects the reponsiveness to oxaliplatin of gastric cancer cells. (A) SGC7901 cells were transfected with sh-L1cam or sramble lentivirus. Cells were left untreated or administrated with different concentrations of oxaliplatin and cell cycle analyses were performed. Graph indicates the percentage of cells in sub G1/G0 phase (apoptotic cells), *P <0.05. (B) HGC27 cells were transfected with L1cam or negative control vectors. Cells were left untreated or administrated with different concentrations of oxaliplatin and cell cycle analyses were performed. Graph indicates the percentage of cells in sub G1/G0 phase (apoptotic cells), *P <0.05.

Mentions: In order to determine if L1cam could affect apoptosis and the responsiveness to anti-cancer drugs in gastric cancer cells, firstly, we analyzed the effect of L1cam on the apoptosis of gastric cancer cells, the results showed that overexpression or knockdown of L1cam had no significant effect on the apoptosis rate in gastric cancer cells (Figure 4A and B); then cells were treated with different concentrations of oxaliplatin, the results showed that knockdown of L1cam could improve the responsiveness to oxaliplatin in SGC7901 cells while overexpression of L1cam could reduce the apoptosis rate in HGC27 cells (P < 0.05, Figure 4A and B).


L1cam promotes tumor progression and metastasis and is an independent unfavorable prognostic factor in gastric cancer.

Chen DL, Zeng ZL, Yang J, Ren C, Wang DS, Wu WJ, Xu RH - J Hematol Oncol (2013)

L1cam affects the reponsiveness to oxaliplatin of gastric cancer cells. (A) SGC7901 cells were transfected with sh-L1cam or sramble lentivirus. Cells were left untreated or administrated with different concentrations of oxaliplatin and cell cycle analyses were performed. Graph indicates the percentage of cells in sub G1/G0 phase (apoptotic cells), *P <0.05. (B) HGC27 cells were transfected with L1cam or negative control vectors. Cells were left untreated or administrated with different concentrations of oxaliplatin and cell cycle analyses were performed. Graph indicates the percentage of cells in sub G1/G0 phase (apoptotic cells), *P <0.05.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3717076&req=5

Figure 4: L1cam affects the reponsiveness to oxaliplatin of gastric cancer cells. (A) SGC7901 cells were transfected with sh-L1cam or sramble lentivirus. Cells were left untreated or administrated with different concentrations of oxaliplatin and cell cycle analyses were performed. Graph indicates the percentage of cells in sub G1/G0 phase (apoptotic cells), *P <0.05. (B) HGC27 cells were transfected with L1cam or negative control vectors. Cells were left untreated or administrated with different concentrations of oxaliplatin and cell cycle analyses were performed. Graph indicates the percentage of cells in sub G1/G0 phase (apoptotic cells), *P <0.05.
Mentions: In order to determine if L1cam could affect apoptosis and the responsiveness to anti-cancer drugs in gastric cancer cells, firstly, we analyzed the effect of L1cam on the apoptosis of gastric cancer cells, the results showed that overexpression or knockdown of L1cam had no significant effect on the apoptosis rate in gastric cancer cells (Figure 4A and B); then cells were treated with different concentrations of oxaliplatin, the results showed that knockdown of L1cam could improve the responsiveness to oxaliplatin in SGC7901 cells while overexpression of L1cam could reduce the apoptosis rate in HGC27 cells (P < 0.05, Figure 4A and B).

Bottom Line: Previous reports have demonstrated that L1cam is aberrantly expressed in various tumors.Ectopic expression of L1cam in gastric cell lines significantly promoted cell proliferation, migration and invasion whereas knockdown of L1cam inhibited cell proliferation, migration and invasion in vitro as well as tumorigenesis and metastasis in vivo.The low level of phosphorylated Akt in HGC27 cells was up-regulated after ectopic expression of L1cam, whereas the high level of phosphorylated Akt in SGC7901 cells was suppressed by knockdown of L1cam.

View Article: PubMed Central - HTML - PubMed

Affiliation: State Key Laboratory of Oncology in South China, Sun Yat-sen University Cancer Center, 651 Dong Feng East Load, Guangzhou 510060, China.

ABSTRACT

Background: Previous reports have demonstrated that L1cam is aberrantly expressed in various tumors. The potential role of L1cam in the progression and metastasis of gastric cancer is still not clear and needs exploring.

Methods: Expression of L1cam was evaluated in gastric cancer tissues and cell lines by immunohistochemistry and Western blot. The relationship between L1cam expression and clinicopathological characteristics was analyzed. The effects of L1cam on cell proliferation, migration and invasion were investigated in gastric cancer cell lines both in vitro and in vivo. The impact of L1cam on PI3K/Akt pathway was also evaluated.

Results: L1cam was overexpressed in gastric cancer tissues and cell lines. L1cam expression was correlated with aggressive tumor phenotype and poor overall survival in gastric cancer patients. Ectopic expression of L1cam in gastric cell lines significantly promoted cell proliferation, migration and invasion whereas knockdown of L1cam inhibited cell proliferation, migration and invasion in vitro as well as tumorigenesis and metastasis in vivo. The low level of phosphorylated Akt in HGC27 cells was up-regulated after ectopic expression of L1cam, whereas the high level of phosphorylated Akt in SGC7901 cells was suppressed by knockdown of L1cam. Moreover, the migration and invasion promoted by L1cam overexpression in gastric cancer cells could be abolished by either application of LY294002 (a phosphoinositide-3-kinase inhibitor) or knockdown of endogenous Akt by small interfering RNA.

Conclusions: Our study demonstrated that L1cam, overexpressed in gastric cancer and associated with poor prognosis, plays an important role in the progression and metastasis of gastric cancer.

Show MeSH
Related in: MedlinePlus