Translational cancer research · 2026
FBXO17 regulates the malignant progression of colorectal cancer via the Wnt/β-catenin pathway.
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Tang Enyan, Xiao Yijie, Qian Xiaohong, Li Shufei, Chen Bin
Аннотация
BACKGROUND: Colorectal cancer (CRC) is one of the most common malignant tumors worldwide, often presenting without apparent early symptoms, and most patients are diagnosed at an advanced stage with a poor prognosis. F-box protein 17 (FBXO17) is up-regulated in various tumors and may represent a potential prognostic marker in CRC. This study sought to elucidate FBXO17's specific role in CRC and the underlying mechanism.
METHODS: Real-time fluorescence quantitative polymerase chain reaction (RT-qPCR), together with Western blot, was applied to determine FBXO17 expression in CRC cell lines. FBXO17-silenced and FBXO17-overexpressing CRC cells were established using a lentiviral system and liposome transfection technology, respectively. Cell counting kit-8, Transwell, and wound healing assays, as well as Western blot, were used to assess CRC cell proliferation, invasion, and migration, and to examine Wnt/β-catenin pathway activation. Intracellular reactive oxygen species (ROS), Fe2+, malondialdehyde (MDA), oxidized glutathione, and reduced glutathione, along with GPX4 and PTGS2 protein expression, were determined to assess CRC cell ferroptosis.
RESULTS: Compared with human normal colon cells, human CRC cells exhibited generally high FBXO17 expression. Silencing FBXO17 led to decreased CRC cell proliferation, invasion, and migration, attenuated Wnt/β-catenin pathway activation, and enhanced ferroptosis, whereas overexpression of FBXO17 reversed these effects by enhancing CRC cell proliferation, invasion, and migration, activating the Wnt/β-catenin pathway, and suppressing ferroptosis. Furthermore, treatment with ferrostatin-1 (ferroptosis inhibitor) or CHIR-99021 (Wnt/β-catenin pathway agonist) enhanced the proliferation, invasion, and migration of FBXO17-silenced CRC cells while attenuating ferroptosis.
CONCLUSIONS: Silencing FBXO17 can promote CRC cell ferroptosis but inhibit proliferation, invasion, and migration through suppression of Wnt/β-catenin pathway activation.
METHODS: Real-time fluorescence quantitative polymerase chain reaction (RT-qPCR), together with Western blot, was applied to determine FBXO17 expression in CRC cell lines. FBXO17-silenced and FBXO17-overexpressing CRC cells were established using a lentiviral system and liposome transfection technology, respectively. Cell counting kit-8, Transwell, and wound healing assays, as well as Western blot, were used to assess CRC cell proliferation, invasion, and migration, and to examine Wnt/β-catenin pathway activation. Intracellular reactive oxygen species (ROS), Fe2+, malondialdehyde (MDA), oxidized glutathione, and reduced glutathione, along with GPX4 and PTGS2 protein expression, were determined to assess CRC cell ferroptosis.
RESULTS: Compared with human normal colon cells, human CRC cells exhibited generally high FBXO17 expression. Silencing FBXO17 led to decreased CRC cell proliferation, invasion, and migration, attenuated Wnt/β-catenin pathway activation, and enhanced ferroptosis, whereas overexpression of FBXO17 reversed these effects by enhancing CRC cell proliferation, invasion, and migration, activating the Wnt/β-catenin pathway, and suppressing ferroptosis. Furthermore, treatment with ferrostatin-1 (ferroptosis inhibitor) or CHIR-99021 (Wnt/β-catenin pathway agonist) enhanced the proliferation, invasion, and migration of FBXO17-silenced CRC cells while attenuating ferroptosis.
CONCLUSIONS: Silencing FBXO17 can promote CRC cell ferroptosis but inhibit proliferation, invasion, and migration through suppression of Wnt/β-catenin pathway activation.