SOCS2 is a potential prognostic marker that suppresses the viability of hepatocellular carcinoma cells
- Jiankun Liu
- Zhiyong Liu
- Wei Li
- Shurong Zhang
Affiliations: Department of Gastroenterology, 920th Hospital of The PLA Joint Logistics Support Force, Kunming, Yunnan 650032, P.R. China, Department of General Surgery, Changzheng Hospital, Second Military Medical University, Shanghai 200003, P.R. China
- Published online on: March 18, 2021 https://doi.org/10.3892/ol.2021.12660
Copyright: © Liu
et al. This is an open access article distributed under the
terms of Creative
Commons Attribution License.
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
This article is mentioned in:
Hepatocellular carcinoma (HCC) is the fourth leading cause of cancer‑associated mortality worldwide. Thus, there is an urgent requirement to identify novel diagnostic and prognostic biomarkers for this disease. The present study aimed to identify the hub genes associated with the progression and prognosis of patients with HCC. A total of three expression profiles of HCC tissues were extracted from the Gene Expression Omnibus (GEO) database, followed by the identification of differentially expressed genes (DEGs) using the GEO2R method. The identified DEGs were assessed for survival significance using Kaplan‑Meier analysis. Among the 15 identified DEGs in HCC tissues [cytochrome P450 family 39 subfamily A member 1, cysteine rich angiogenic inducer 61, Fos proto‑oncogene, forkhead transcription factor 1 (FOXO1), growth arrest and DNA damage inducible β, Inhibitor of DNA binding 1, interleukin‑1 receptor accessory protein, metallothionein‑1M, pleckstrin homology‑like domain family A member 1, Rho family GTPase 3, serine dehydratase, suppressor of cytokine signaling 2 (SOCS2), tyrosine aminotransferase (TAT), S100 calcium‑binding protein P and serine protease inhibitor Kazal‑type 1 (SPINK1)]. Low expression levels of FOXO1, SOCS2 and TAT and high SPINK1 expression indicated poor survival outcomes for patients with HCC. In addition, SOCS2 was associated with distinct stages of HCC progression in patients and presented optimal diagnostic value. In vitro functional experiments indicated that overexpression of SOCS2 inhibited HCC cell proliferation and migration. Taken together, the results of the present study suggest that SOCS2 may act as a valuable prognostic marker that is closely associated with HCC progression.