Increased Expression of 58-kDa Microspherule Protein (MSP58) in Human Gastric Cancer Promotes Cell Proliferation and Correlates with Poor Patient Survival.
2016
Abstract Gastric cancer (GC) is one of the most frequently occurring malignancies with poor prognosis because of its huge heterogeneity and limited available therapeutic options. The nucleolar 58-kDa microspherule protein (MSP58) is involved in a variety of cellular processes. Though MSP58 was identified as a candidate oncogene in many cancer types, it has both oncogenic and tumor suppressive properties. The oncogenic effect of MSP58 in GC is currently unclear. The present study identified MSP58 expression in GCs and investigated its role in tumor proliferation and patient survival. MSP58 expression in GCs was identified using western blotting and immunochemistry methods and correlations with clinicopathological features. Patient survival was calculated by multivariate survival analysis. Small interference RNA transfection, CCK8, and clonogenic assays were performed to investigate the roles of MSP58 in cell proliferation. MSP58 was highly expressed in MGC803, BGC823, and NCI-N87 cell lines compared with normal gastric mucosa cells. The study thus provided evidence that knockdown of MSP58 expression significantly suppressed cell proliferation and colony-forming ability. Immunohistochemical analysis showed MSP58 was highly expressed in 51.5% of GC tissues and in 11.9% of normal corresponding mucosal tissues. Significant positive correlations between MSP58 expression and differentiation grade, depth of invasion, and pathological tumor node metastasis (TNM) stage was further identified. The overall 5-year survival rate for the MSP58-positive group was lower than that of the MSP58-negative group. Depth of invasion, lymph node metastasis, and MSP58 expression were found to be independent prognostic factors. These findings suggested that MSP58 plays an important role in tumorigenesis and progression and may help predict the prognosis of GC patients.
Keywords:
- Correction
- Source
- Cite
- Save
- Machine Reading By IdeaReader
0
References
2
Citations
NaN
KQI