CXCL17 promotes cell metastasis and inhibits autophagy via the LKB1-AMPK pathway in hepatocellular carcinoma.

07:00 EST 28th December 2018 | BioPortfolio

Summary of "CXCL17 promotes cell metastasis and inhibits autophagy via the LKB1-AMPK pathway in hepatocellular carcinoma."

As an innovative CXC chemokine, CXCL17 has a mysterious clinical significance and modulating influence on hepatocellular carcinoma (HCC). Our study examined the activity and mechanisms of CXCL17 on growth, autophagy, and metastasis of HCC. Upregulation of CXCL17 expression was observed in HCC, which is correlated with poorer histological stages and outcomes. Elevation of CXCL17 expression promoted proliferation, invasion, and migration and decreased LC-3B biosynthesis and p62 protein reduction, which are known to stimulate autophagy. However, silencing of CXCL17 inhibited the development of these cancerous phenotypes. Furthermore, AMPK was stimulated after knockdown of CXCL17. This stimulation, as well as stimulation of autophagy was caused by liver kinase B1 (LKB1), whose function is induced by knockdown CXCL17. Additionally, knockdown of CXCL17 enhanced nuclear translocation of LKB1. Altogether, these findings suggest that elevated CXCL17 expression in HCC promotes malignant reactions in malignant cells. Our research offers new evidence that chemokine CXCL17 reinforces malignant invasion and suppresses autophagy via the LKB1-AMPK pathway.


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This article was published in the following journal.

Name: Gene
ISSN: 1879-0038


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Medical and Biotech [MESH] Definitions

A serine/threonine-protein kinase that functions in AUTOPHAGY in response to starvation. It acts on the PHOSPHATIDYLINOSITOL 3-KINASE complex PIK3C3 to regulate AUTOPHAGOSOME formation. It also functions as both a downstream effector and negative regulator of mammalian target of rapamycin complex 1 (mTORC1) and is activated by AMPK, which it also negatively regulates.

An autophagy related protein that is similar to UBIQUITIN-ACTIVATING ENZYME E1. It functions in CYTOPLASM to VACUOLE transport (Cvt) and AUTOPHAGY by activating ATG12 PROTEIN for its conjugation with ATG5 PROTEIN, as well as the conjugation of ATG8 FAMILY PROTEINS with phosphatidylethanolamine for ATG8 association to Cvt vesicles and AUTOPHAGOSOME membranes. It is also required for the nitrogen starvation response in yeast, MITOPHAGY; and autophagic cell death induced by CASPASE 8 inhibition.

Proteins and enzymes that function, often as components of MULTIPROTEIN COMPLEXES, to assemble AUTOPHAGOSOMES and carry out AUTOPHAGY.

Surface ligands, usually glycoproteins, that mediate cell-to-cell adhesion. Their functions include the assembly and interconnection of various vertebrate systems, as well as maintenance of tissue integration, wound healing, morphogenic movements, cellular migrations, and metastasis.

Ubiquitous macromolecules associated with the cell surface and extracellular matrix of a wide range of cells of vertebrate and invertebrate tissues. They are essential cofactors in cell-matrix adhesion processes, in cell-cell recognition systems, and in receptor-growth factor interactions. (From Cancer Metastasis Rev 1996; 15(2): 177-86; Hepatology 1996; 24(3): 524-32)

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