ArticleWorld journal of surgery2018
Analysis of Potential Alterations Affecting SETBP1 as a Novel Contributing Mechanism to Inhibit PP2A in Colorectal Cancer Patients.
Article in World journal of surgery, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 16 citations in OpenAlex.
- SET-binding protein 1 (SETBP1) suppresses cell proliferation in estrogen receptor-positive breast cancer.Breast cancer (Tokyo, Japan) · 2025Article
- Mutational disparities in colorectal cancers of White Americans, Alabama African Americans, And Oklahoma American Indians.NPJ precision oncology · 2024Article
- The mLeukemia · 2024Article
- SETBP1 activation upon MDM4-enhanced ubiquitination of NR3C1 triggers dissemination of colorectal cancer cells.Clinical & experimental metastasis · 2024Article
- Identification of a chromatin regulator signature and potential candidate drugs for bladder cancer.Hereditas · 2022Article
- Comprehensive analysis of mFrontiers in oncology · 2022Article
- The Role of SETBP1 in Gastric Cancer: Friend or Foe.Frontiers in oncology · 2022Article
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Authors and funding
12 authors at 2 institutions in 1 country.
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Abstract
backgroundThe functional loss of the tumor suppressor protein phosphatase 2A (PP2A) occurs in a wide variety of human cancers including colorectal cancer (CRC), and SET overexpression has been reported as a key contributing mechanism to inhibit PP2A. Although SET binding protein 1 (SETBP1) overexpression and gain of function mutations have been described in several hematological malignancies as common events that increase the expression levels of the PP2A inhibitor SET, thereby leading to PP2A inactivation, the potential existence of SETBP1 alterations in CRC still remains unexplored.
methodsWe studied the expression profile of SETBP1 by Western blot in a set of CRC cell lines and patient samples. Moreover, we performed co-immunoprecipitation assays to analyze the formation of the previously reported SETBP1-SET-PP2A inhibitory complex. Furthermore, we evaluated the mutational status of SETBP1 by pyrosequencing assays in a cohort of 55 CRC patients with metastatic disease after the immunohistochemical characterization of SET and p-PP2A expression in this cohort.
resultsWe found high SETBP1 expression in several CRC lines but only in two of the patients analyzed. In addition, we demonstrated the formation of the SETBP1-SET-PP2A heterotrimeric complex in CRC cells. However, we failed to detect SETBP1 mutations in any of the CRC patient samples included in the study.
conclusionsOur results suggest that SETBP1 expression is mainly similar o lower in colorectal cancer tissue compared to normal colonic mucosa. However, its overexpression is a low prevalent alteration which could contribute to inhibit PP2A in CRC through the formation of a SETBP1-SET-PP2A complex in some CRC patients. Moreover, SETBP1 mutations are, if exist, rare events in CRC patients.
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