ArticleMedical oncology (Northwood, London, England)2013
Expression of MSP58 in hepatocellular carcinoma.
Article in Medical oncology (Northwood, London, England), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 18 citations in OpenAlex.
- MCRS1 Expression Regulates Tumor Activity and Affects Survival Probability of Patients with Gastric Cancer.Diagnostics (Basel, Switzerland) · 2022Article
- Mcrs1 interacts with Six1 to influence early craniofacial and otic development.Developmental biology · 2020Article
- Expression of MCRS1 and MCRS2 and their correlation with serum carcinoembryonic antigen in colorectal cancer.Experimental and therapeutic medicine · 2016Article
- MCRS1 associates with cytoplasmic dynein and mediates pericentrosomal material recruitment.Scientific reports · 2016Article
- Using Xenopus to discover new genes involved in branchiootorenal spectrum disorders.Comparative biochemistry and physiology. Toxicology & pharmacology : CBP · 2015Review
- The candidate oncogene (MCRS1) promotes the growth of human lung cancer cells via the miR-155-Rb1 pathway.Journal of experimental & clinical cancer research : CR · 2015Article
- MCRS1 overexpression, which is specifically inhibited by miR-129*, promotes the epithelial-mesenchymal transition and metastasis in non-small cell lung cancer.Molecular cancer · 2014Article
- The molecular characteristics and functional roles of microspherule protein 1 (MCRS1) in gene expression, cell proliferation, and organismic development.Cell cycle (Georgetown, Tex.)Review
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have investigated the expression and role of the 58-kDa micro-spherule protein (MSP58) in hepatocellular carcinoma (HCC). Immunohistochemistry was performed in 252 samples from patients with HCC to detect the expression level of MSP58. Results indicated that the expression level of MSP58 in the cancer samples was significantly higher than that in adjacent normal tissues. The Wilcoxon-Mann-Whitney test showed significant difference in the expression of MSP58 in patients with serum AFP, tumor size, histological differentiation, and universal integrated circuit card (UICC) stage (P < 0.001, P = 0.004, P < 0.001, P < 0.001, respectively). A total of 252 HCC patients were followed up for five consecutive years, and Kaplan-Meier survival analysis demonstrated that the survival time of HCC patients with low expression of MSP58 was longer than those with high expression during the 5-year follow-up period (P < 0.001). Cox regression analysis indicated that high expression of MSP58 (++ or +++), serum AFP (≥25 μg/L), tumor size (≥3 cm), and UICC stage (III or IV) were the independent poor prognostic factors of HCC (P = 0.008, 0.0290, 0.001, 0.047, respectively). Furthermore, down-regulation of MSP58 was introduced to HCC cell lines (HepG2 and Huh7) by plasmid transfection. In vivo and in vitro studies indicated that MSP58si markedly reduced proliferation and promoted the apoptosis of HepG2 and Huh7 cells. In summary, our results demonstrated that MSP58 played an important role in the proliferation and apoptosis of HCC cells and the expression of MSP58 in HCC patients was closely related to the prognosis.
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