GOLPH3-STIP1 Complex Activates STAT3 Through Exosome Secretion to Induce Colon Cancer Metastasis.

With a high mortality rate, colon cancer (CC) is the third most common malignant tumor worldwide. The primary causes are thought to be the high invasiveness and migration of CC cells. The functions of Golgi phosphoprotein 3 (GOLPH3), stress-induced phosphoprotein 1 (STIP1), and the signal transducer and activator of transcription 3 (STAT3) signaling pathway in the invasion and migration of CC cells were examined in this study.

Gastrointestinal toxicities associated with immune checkpoint inhibitors: a disproportionality analysis leveraging VigiBase, the WHO Adverse Drug Reaction Database.

With the improvement of people's living standards, gastrointestinal adverse reactions caused by various adverse factors have attracted more and more people's attention. A recent study has indicated that coronavirus disease 2019 (COVID-19) could also invade the gastrointestinal tract, leading to gastrointestinal adverse reactions (Song et al., 2020).

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).