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Up-regulation of SLC9A9 Promotes Cancer Progression and Is Involved in Poor Prognosis in Colorectal Cancer.
- Source :
-
Anticancer research [Anticancer Res] 2017 May; Vol. 37 (5), pp. 2255-2263. - Publication Year :
- 2017
-
Abstract
- Background/aim: SLC9A9 plays an oncogenic role in esophageal squamous carcinoma and glioblastoma. Herein, we showed an oncogenic function of SLC9A9 in colorectal cancer (CRC).<br />Materials and Methods: We examined SLC9A9 expression in CRC specimens by immunohistochemistry. In CRC tissues, the relationship between SLC9A9 expression and clinicopathological factors was further elucidated by quantitative real-time polymerase chain reaction (qRT-PCR) and gene set enrichment analysis (GSEA). In vitro, we performed knockdown and overexpression experiments.<br />Results: SLC9A9 was overexpressed in CRC specimens. In clinicopathological analysis of our cohort, high SLC9A9 expression increased liver metastasis and was correlated with worse prognoses in two cohorts. A significantly positive relationship between SLC9A9 and EGFR was revealed. While knockdown of SLC9A9 suppressed proliferation and anchorage-independent growth, up-regulation of SLC9A9 promoted proliferation and anchorage-independent growth in vitro.<br />Conclusion: SLC9A9 has an oncogenic function by being related to EGFR signaling, suggesting SLC9A9 may be a novel prognostic indicator and a therapeutic target in CRC.<br /> (Copyright© 2017, International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.)
- Subjects :
- Aged
Cell Line, Tumor
Colorectal Neoplasms genetics
Colorectal Neoplasms pathology
Disease Progression
ErbB Receptors genetics
Female
Gene Expression Regulation, Neoplastic
Humans
Male
Prognosis
RNA, Messenger genetics
RNA, Small Interfering genetics
Sodium-Hydrogen Exchangers genetics
Up-Regulation
Colorectal Neoplasms metabolism
ErbB Receptors metabolism
Sodium-Hydrogen Exchangers metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 1791-7530
- Volume :
- 37
- Issue :
- 5
- Database :
- MEDLINE
- Journal :
- Anticancer research
- Publication Type :
- Academic Journal
- Accession number :
- 28476790
- Full Text :
- https://doi.org/10.21873/anticanres.11562