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Down-regulated expression of OPCML predicts an unfavorable prognosis and promotes disease progression in human gastric cancer

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ABSTRACT

Background: OPCML belongs to the IgLON family of Ig domain–containing GPI-anchored cell adhesion molecules and was recently found to be involved in carcinogenesis, while its role in gastric cancer remains unclear.

Methods: We assessed expression and biological behavior of OPCML in gastric cancer.

Results: OPCML expression was markedly reduced in tumor tissues and cancer cell lines. Decreased OPCML expression had a significant association with unfavorable tumor stage (p = 0.007) and grading (p < 0.001). Furthermore, the results revealed that OPCML was an independent prognostic factor for overall survival in gastric cancer (p = 0.002). In addition, ectopic expression of OPCML in cancer cells significantly inhibited cell viability (p < 0.01) and colony formation (p < 0.001), arrest cell cycle in G0/G1 phase and induced apoptosis, and suppressed tumor formation in nude mice. The alterations of phosphorylation status of AKT and its substrate GSK3β, up-regulation of pro-apoptotic regulators including caspase-3, caspase-9 and PARP, and up-regulation of cell cycle regulator p27, were implicated in the biological activity of OPCML in cancer cells.

Conclusion: Down-regulated OPCML expression might serve as an independent predictor for unfavorable prognosis of patients, and the biological behavior supports its role as a tumor suppressor in gastric cancer.

Electronic supplementary material: The online version of this article (doi:10.1186/s12885-017-3203-y) contains supplementary material, which is available to authorized users.

No MeSH data available.


Related in: MedlinePlus

OPCML was decreased or lost by promoter methylation in gastric cells (a) and (b) The significant reduction of OPCML mRNA expression by real-time PCR and protein expression by western blot in seven gastric cancer cell lines, compared with normal stomach tissues. c OPCML mRNA expression by RT-PCR and promoter methylation by MSP in gastric cancer cell lines. d Changes of OPCML mRNA expression in gastric cancer cell lines after 5-aza-2′-deoxycytidine treatment. D: DMSO; A: 5-aza-2′-deoxycytidine. * P < 0.0001
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Fig2: OPCML was decreased or lost by promoter methylation in gastric cells (a) and (b) The significant reduction of OPCML mRNA expression by real-time PCR and protein expression by western blot in seven gastric cancer cell lines, compared with normal stomach tissues. c OPCML mRNA expression by RT-PCR and promoter methylation by MSP in gastric cancer cell lines. d Changes of OPCML mRNA expression in gastric cancer cell lines after 5-aza-2′-deoxycytidine treatment. D: DMSO; A: 5-aza-2′-deoxycytidine. * P < 0.0001

Mentions: We detected the expression of OPCML in seven gastric cancer cell lines. The results showed that expressions of both OPCML mRNA and protein were markedly down-regulated or lost in all seven gastric cancer cell lines, while it is readily detectable in the normal stomach tissues (Fig. 2a, b).Fig. 2


Down-regulated expression of OPCML predicts an unfavorable prognosis and promotes disease progression in human gastric cancer
OPCML was decreased or lost by promoter methylation in gastric cells (a) and (b) The significant reduction of OPCML mRNA expression by real-time PCR and protein expression by western blot in seven gastric cancer cell lines, compared with normal stomach tissues. c OPCML mRNA expression by RT-PCR and promoter methylation by MSP in gastric cancer cell lines. d Changes of OPCML mRNA expression in gastric cancer cell lines after 5-aza-2′-deoxycytidine treatment. D: DMSO; A: 5-aza-2′-deoxycytidine. * P < 0.0001
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC5391589&req=5

Fig2: OPCML was decreased or lost by promoter methylation in gastric cells (a) and (b) The significant reduction of OPCML mRNA expression by real-time PCR and protein expression by western blot in seven gastric cancer cell lines, compared with normal stomach tissues. c OPCML mRNA expression by RT-PCR and promoter methylation by MSP in gastric cancer cell lines. d Changes of OPCML mRNA expression in gastric cancer cell lines after 5-aza-2′-deoxycytidine treatment. D: DMSO; A: 5-aza-2′-deoxycytidine. * P < 0.0001
Mentions: We detected the expression of OPCML in seven gastric cancer cell lines. The results showed that expressions of both OPCML mRNA and protein were markedly down-regulated or lost in all seven gastric cancer cell lines, while it is readily detectable in the normal stomach tissues (Fig. 2a, b).Fig. 2

View Article: PubMed Central - PubMed

ABSTRACT

Background: OPCML belongs to the IgLON family of Ig domain&ndash;containing GPI-anchored cell adhesion molecules and was recently found to be involved in carcinogenesis, while its role in gastric cancer remains unclear.

Methods: We assessed expression and biological behavior of OPCML in gastric cancer.

Results: OPCML expression was markedly reduced in tumor tissues and cancer cell lines. Decreased OPCML expression had a significant association with unfavorable tumor stage (p&nbsp;=&nbsp;0.007) and grading (p&nbsp;&lt;&nbsp;0.001). Furthermore, the results revealed that OPCML was an independent prognostic factor for overall survival in gastric cancer (p&nbsp;=&nbsp;0.002). In addition, ectopic expression of OPCML in cancer cells significantly inhibited cell viability (p&nbsp;&lt;&nbsp;0.01) and colony formation (p&nbsp;&lt;&nbsp;0.001), arrest cell cycle in G0/G1 phase and induced apoptosis, and suppressed tumor formation in nude mice. The alterations of phosphorylation status of AKT and its substrate GSK3&beta;, up-regulation of pro-apoptotic regulators including caspase-3, caspase-9 and PARP, and up-regulation of cell cycle regulator p27, were implicated in the biological activity of OPCML in cancer cells.

Conclusion: Down-regulated OPCML expression might serve as an independent predictor for unfavorable prognosis of patients, and the biological behavior supports its role as a tumor suppressor in gastric cancer.

Electronic supplementary material: The online version of this article (doi:10.1186/s12885-017-3203-y) contains supplementary material, which is available to authorized users.

No MeSH data available.


Related in: MedlinePlus