Chondroitin polymerizing factor promotes breast carcinoma cell proliferation, invasion and migration and affects expression of epithelial‐mesenchymal transition‐related markers

Abstract

Chondroitin polymerizing factor (CHPF) plays an important role in the development of certain malignant tumors. However, the role of CHPF in breast carcinoma (BRCA) and its underlying mechanism are still not fully elucidated. Expression profiles for CHPF in BRCA tissues were retrieved from The Cancer Genome Atlas database and used for prognostic analysis. Cell viability, invasion and migration were measured in vitro using MCF7 and MDA-MB-231 cell lines upon knockdown or over-expression of CHPF. Bioinformatic analysis showed that CHPF was substantially upregulated in BRCA tissues, and a quantitative reverse transcriptase-PCR was performed to confirm its upregulation in BRCA cells. High expression of CHPF was observed to be significantly associated with pathologic stage, metastasis and worse prognosis. We also observed that depletion of CHPF significantly inhibited cell proliferative, invasive and migratory abilities, whereas overexpression of CHPF exerted the opposite effects. Furthermore, analysis of the GEPIA database revealed that CHPF expression is positively correlated with the epithelial-mesenchymal transition-related markers vimentin, Snail, Slug and motion-related protein matrix metallopeptidase 2; these findings were confirmed via western blotting. Our data suggest that CHPF may contribute to BRCA progression by modulating epithelial-mesenchymal transition-related markers and matrix metallopeptidase 2 expression. Breast carcinoma (BRCA) is the most commonly diagnosed cancer in women and ranks the second among causes of cancer relative death in women [1]. Globally, the incidence rate of BRCA has been rising rapidly

Four Immune-Related Genes (FN1, UGCG, CHPF2 and THBS2) as Potential Diagnostic and Prognostic Biomarkers for Carbon Nanotube-Induced Mesothelioma

“…46,47 High expression of CHPF was significantly associated with pathologic stage, metastasis and worse prognosis of breast carcinoma patients. 48 In line with these studies, our results also showed FN1, THBS2, CSPG4 and CHPF were 4), indirectly providing an evidence to show the oncogenic functions of CHPF2 in MPM. UGCG is the only enzyme for the synthesis of glucosylceramide via transferring a UDP-glucose molecule to ceramide.…”

“… 46 , 47 High expression of CHPF was significantly associated with pathologic stage, metastasis and worse prognosis of breast carcinoma patients. 48 In line with these studies, our results also showed FN1, THBS2, CSPG4 and CHPF were upregulated in CNT-induced malignant transformed MeT5A cells, mice and MPM tissues, associated with OS and enriched in extracellular matrix-related biological process and pathways. Although no study demonstrated the roles of CHPF2 in cancer, CHPF2 was predicted to interact with CSPG4 and CHPF in our PPI network ( Figure 4 ), indirectly providing an evidence to show the oncogenic functions of CHPF2 in MPM.…”

A Novel Prognostic Signature Based on Metabolism-Related Genes to Predict Survival and Guide Personalized Treatment for Head and Neck Squamous Carcinoma

“…CHPF2 acts as an oncogene that is up-regulated in cancers to exert its positive role in cell proliferation and metastasis, including breast cancer, hepatocellular carcinoma, lung adenocarcinoma, etc. (29)(30)(31). CYP4X1, a member of the cytochromes P450 family, oxidatively metabolizes a wide range of physiological substrates and plays a potential role in the body in response to cancer chemotherapy (32).…”

Characterization of glucose metabolism in breast cancer to guide clinical therapy

“…CHPF is highly expressed in lung adenocarcinoma and can promote tumor cell growth, invasion and metastasis, and inhibit tumor cell apoptosis ( 43 ). More specifically, the role of CHPF in breast cancer is to promote proliferation, invasion and migration ( 44 ). IRS2 is an insulin-like growth factor-1 receptor (IGF-1R) and insulin receptor signaling transmitter, which may be involved in the PI3K-AKT pathway, leading to the occurrence and progression of malignant tumors and inhibition of apoptosis ( 45 , 46 ).…”