Abstract
BackgroundEsophageal cancer is one of the most aggressive malignancies, and is associated with multiple genetic mutations. At present, the v-Raf murine sarcoma viral oncogene homolog B1 (BRAF) gene mutation has been observed in esophageal cancer and is associated with poor prognosis. This study aimed to investigate the protein expression of BRAF in esophageal cancer and determine its effect on patient outcomes.MethodsWe used immunohistochemistry to detect the expression of BRAF via tissue microarrays in esophageal cancer samples, the Kaplan–Meier method to perform survival analysis, and the Cox proportional hazards regression model to explore the risk factors of esophageal cancer. The role of BRAF in the proliferation, invasion, and metastasis of esophageal cancer was studied by clone formation, scratch test, Transwell invasion and migration test. The tumor-bearing model of BRAF inhibitor was established using TE-1 cells, and corresponding negative control was set up to observe the growth rate of the two models.ResultsThe results revealed that BRAF overexpression was significantly correlated with Ki67 (P < 0.05). Survival analysis showed that BRAF overexpression contributed to a shorter overall survival (P = 0.014) in patients with esophageal cancer. Univariate and multivariate regression analyses demonstrated that BRAF was a prognostic factor for poor esophageal cancer outcomes (P < 0.05). Small interfering RNA knockdown of BRAF significantly reduced the cell clone formation rate compared to the control group. Transwell assay analysis showed that the migration and invasion of cells in the experimental group were significantly inhibited relative to the control group, and the inhibition rates of the small interfering RNA group were 67% and 60%, respectively. In the scratch test, the wound healing ability of the BRAF knockdown group was significantly weaker than that of the control group. There were significant differences in tumor growth volume and weight between the two groups in nude mice.ConclusionBRAF overexpression may serve as an effective predictive factor for poor prognosis.
Highlights
Esophageal cancer is one of the most aggressive malignancies, and is associated with multiple genetic mutations
The coding products of v-Raf murine sarcoma viral oncogene homolog B1 (BRAF) occur through the epidermal growth factor receptor (EGFR) signal transduction network, which plays a crucial role in multiple tumorigenic processes, including cell cycle progression, angiogenesis, metastasis, and protection of the cancer cell from apoptosis [4, 5]
Mutations in the Kirsten ras 1 (KRAS) and V-Raf murine sarcoma viral oncogene homolog B1 (BRAF) genes may be predictive of drug responses that are directly linked to the EGFR pathway [6]
Summary
Esophageal cancer is one of the most aggressive malignancies, and is associated with multiple genetic mutations. The v-Raf murine sarcoma viral oncogene homolog B1 (BRAF) gene mutation has been observed in esophageal cancer and is associated with poor prognosis. This study aimed to investigate the protein expression of BRAF in esophageal cancer and determine its effect on patient outcomes. The coding products of v-Raf murine sarcoma viral oncogene homolog B1 (BRAF) occur through the epidermal growth factor receptor (EGFR) signal transduction network, which plays a crucial role in multiple tumorigenic processes, including cell cycle progression, angiogenesis, metastasis, and protection of the cancer cell from apoptosis [4, 5]. Mutations in the Kirsten ras 1 (KRAS) and BRAF genes may be predictive of drug responses that are directly linked to the EGFR pathway [6]
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