Expression and Clinical Significance of Golgi Phosphoprotein 3 (GOLPH3) in Papillary Thyroid Carcinoma.

This study aimed to explore the correlation of Golgi phosphoprotein 3 (GOLPH3) levels in papillary thyroid carcinoma (PTC) and papillary thyroid microcarcinoma (PTMC) with clinicopathologic features. GOLPH3 expression was determined by western blotting in solid tumors and the adjacent normal thyroid tissues. Mammalian target of rapamycin (mTOR) and Ki-67 were examined by immunohistochemical staining.

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.

Silencing GOLPH3 gene expression reverses resistance to cisplatin in HT29 colon cancer cells via multiple signaling pathways.

Golgi phosphorylated protein (GOLPH)3 is overexpressed in colorectal cancer tissues and promotes the proliferation of colon cancer cells. A previous study by the authors demonstrated that GOLPH3 was associated with poor prognosis in colorectal cancer. However, the association between GOLPH3 gene overexpression and resistance to platinum-based drugs in colon cancer remains unknown.

GOLPH3 expression promotes the resistance of HT29 cells to 5‑fluorouracil by activating multiple signaling pathways.

The novel proto‑oncogene Golgi phosphoprotein (GOLPH)3 is overexpressed in a variety of tumor tissues and is associated with poor prognosis. The authors previously demonstrated that GOLPH3 gene is overexpressed in colorectal cancer tissues and promotes the proliferation of colonic cancer cells by activating the phosphatidylinositol‑3‑kinase/protein kinase B/the mammalian target of rapamycin and Wnt/β‑catenin signaling pathways. However, to the best of the authors' knowledge, if and how the GOLPH3 gene is involved in inducing resistance to colonic cancer chemotherapy has not been reported.

Correlation of GOLPH3 Gene with Wnt Signaling Pathway in Human Colon Cancer Cells.

Objective: Overexpression of GOLPH3 in colorectal cancer tissue may promote cell proliferation and activate the Wnt signaling pathway. We investigated the correlation between GOLPH3 gene expression and the Wnt signaling pathway to explore the mechanism of the overexpression of GOLPH3 gene which promotes proliferation in human colon cancer cells.

Methods: We measured expression of GOLPH3 mRNA in the human colon cancer cell lines HCT116, HT29, SW480 and SW620 by RT-PCR, and the cells with the highest expression were selected and divided into four groups: negative control, GOLPH3 siRNA transfection (siRNA-GOLPH3), Akt inhibitor (Tricinbine), and glycogen synthase kinase (GSK)-3β inhibitor (TWS119).

Correlational research of Golgi phosphorylation protein 3 expression in colorectal cancer.

Aim: To investigate the effect of Golgi phosphorylation protein 3 (GOLPH3) expression on cell apoptosis, angiogenesis and prognosis in colorectal cancer (CRC).

Methods: The expression of GOLPH3 in CRC tissues and normal colorectal mucosae was determined by immunohistochemistry in 62 patients. In addition, immunohistochemistry was also carried out to detect the expression of vascular endothelial growth factor (VEGF), CD34 and microvessel density (MVD).