Literature DB >> 28482619

14-3-3σ downregulation suppresses ICC metastasis via impairing migration, invasion, and anoikis resistance of ICC cells.

Zhenjie Yang1,2,1, Qianjun Jin1,3,1, Wendi Hu1,2, Longfei Dai1,2, Zhengze Xue1,3, Da Man2, Lin Zhou2,4, Haiyang Xie2,4, Jian Wu1,4, Shusen Zheng1,2,4.   

Abstract

BACKGROUND: 14-3-3σ protein plays an important role in multiple cellular processes. The role of 14-3-3σ in the progression of intrahepatic cholangiocarcinoma (ICC) has not been well understood.
OBJECTIVE: We performed this research to explore the relationship between 14-3-3σ level and clinical characteristics and prognosis of ICC patients. Besides, we used ICC cell lines HCCC-9810 and RBE to assess the biological function of 14-3-3σ.
METHODS: We examined 14-3-3σ expression in 28 ICC tissues and matched paratumor tissues by quantitative real-time PCR and immunohistochemistry. Additionally, ICC tissue array from 100 patients and normal liver tissue array from 24 healthy people were also analyzed by immunohistochemistry. 14-3-3σ was knocked down in ICC cell lines and the functions and mechanisms of 14-3-3σ were assessed.
RESULTS: 14-3-3σ is highly expressed in ICC tissues and high expression of 14-3-3σ correlates poor overall survival in ICC patients. Knocking down of 14-3-3σ in ICC cell lines reduced cells migration, invasion and anoikis resistance. Furthermore, 14-3-3σ-silenced ICC cells showed significantly decreased invasion-related protein MMP2 and MMP9 expression.
CONCLUSIONS: Our results demonstrate prognostic value of 14-3-3σ and its role in metastasis, which is associated with ICC cell lines migration, invasion and anoikis resistance.

Entities:  

Keywords:  14-3-3σ intrahepatic cholangiocarcinoma; anoikis resistance; metastasis

Mesh:

Substances:

Year:  2017        PMID: 28482619     DOI: 10.3233/CBM-160476

Source DB:  PubMed          Journal:  Cancer Biomark        ISSN: 1574-0153            Impact factor:   4.388


  1 in total

1.  The 14-3-3σ protein promotes HCC anoikis resistance by inhibiting EGFR degradation and thereby activating the EGFR-dependent ERK1/2 signaling pathway.

Authors:  Jia Song; Yachong Liu; Furong Liu; Lu Zhang; Ganxun Li; Chaoyi Yuan; Chengpeng Yu; Xun Lu; Qiumeng Liu; Xiaoping Chen; Huifang Liang; Zeyang Ding; Bixiang Zhang
Journal:  Theranostics       Date:  2021-01-01       Impact factor: 11.556

  1 in total

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