HCRP‑1 alleviates the malignant phenotype and angiogenesis of oral squamous cell carcinoma cells via the downregulation of the EGFR/STAT3 signaling pathway

Abstract

It has previously been reported that human hepatocellular carcinoma-related protein 1 (HCRP-1), which is a tumor suppressor gene, and epidermal growth factor receptor (EGFR) are abnormally expressed in certain solid tumors. Therefore, in the present study, the expression patterns of HCRP-1 in oral squamous cell carcinoma (OSCC) are discussed. Moreover, the present study investigated whether HCRP-1 regulated EGFR expression levels and its downstream effectors to further determine the regulation of tumor cell behavior. Therefore, the expression levels of HCRP-1 in normal oral epithelial and OSCC cells were determined, and the effects of HCRP-1 overexpression on OSCC cell proliferation, migration and invasion were assessed. Moreover, the culture medium from the different groups of OSCC cells was separately supplemented into the human umbilical vein endothelial cell (HUVEC) cultures, and the migration and angiogenesis of the HUVECs were assessed. To determine the roles of EGFR/STAT3 in the regulation of HCRP-1, EGF and colivelin, a STAT3 agonist, were used to treat CAL-27 cells and their effects on the cells were assessed using the aforementioned functional experiments. The results demonstrated that HCRP-1 expression levels were downregulated in OSCC cells and that HCRP-1 overexpression could suppress OSCC cell proliferation, migration and invasion. Moreover, the culture medium from OSCC cells overexpressing HCRP-1 facilitated the migration and angiogenesis of HUVECs. Furthermore, HCRP-1 was demonstrated to function in cells by regulating the EGFR/STAT3 signaling pathway. In summary, the present study indicated that HCRP-1 alleviated the malignant phenotype and angiogenesis of OSCC cells via the downregulation of the EGFR/STAT3 signaling pathway.

Rauwolfia polysaccharide can inhibit the progress of ulcerative colitis through NOS2-mediated JAK2/STAT3 pathway

“…Also, as the concentration of colivelin increased, STAT3 and p-STAT3 expression increased significantly ( Fig 6B–6D ). According to the related articles [ 22 , 23 ], we finally selected 1μM colivelin for follow-up experiments.…”

Dendrobine regulates STAT3 to attenuate mitochondrial dysfunction and senescence in vascular endothelial cells triggered by oxidized low‐density lipoprotein

“…Human umbilical vein endothelial cells (HUVECs; ATCC) were cultured with EC medium (Sigma‐Aldrich) containing fetal bovine serum and penicillin/streptomycin, and the culture dish was placed at 37°C in a 5% CO 2 environment. The cells were treated with ox‐LDL (10 μg/mL) for 48 h to mimic AS, and pretreated with dendrobine (10 μM; Herbpurify) for 12 h. In the follow‐up mechanism study, cells were stimulated with mitophagy inhibitor Mdivi‐1 (10 μM; Selleck) for 2 h (Huang et al, 2022) or STAT3 agonist colivelin (1 μM; Selleck) for 24 h (Chen & Hou, 2022).…”