Expert review of anticancer therapy · 2024
Activation of ferritin light chain (FTL) by transcription factor salmonella pathogenicity island 1 modulates glycolysis to drive metastasis of ovarian cancer cells.
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Li Chunxiang, Yang Yubin, Lin Yuting, Lian Yingbin, Pan Dinglong, Lin Lin, Li Luhong
Аннотация
BACKGROUND: Ovarian cancer (OC) is the most lethal gynecological cancer often diagnosed at an advanced stage due to a lack of effective biomarkers. Ferritin light chain (FTL) is implicated in the development of various cancers, but its impact on OC remains unknown.
RESEARCH DESIGN AND METHODS: Bioinformatics methods were utilized to analyze FTL. Quantitative real-time polymerase chain reaction, western blot, and immunohistochemistry were employed for expression detection, and cell counting kit- 8, and transwell assays were for cell biological functions assessment. Extracellular acidification rate, oxygen consumption rate, and glycolytic metabolite contents were measured. Dual-luciferase and chromatin immunoprecipitation assay validated binding relationship. Xenografted tumor models in nude mice verified the role of FTL in vivo.
RESULTS: Cell function experiments revealed that FTL facilitated proliferation, migration, and invasion of OC cells. Rescue experiments unveiled that 2-Deoxy-D-glucose attenuated stimulation on OC cell metastasis and glycolysis by FTL overexpression. Salmonella pathogenicity island 1 (SPI1) up-regulated FTL expression to promote glycolysis and metastasis. FTL knockdown inhibited tumor growth and suppressed glycolysis and cell metastasis in vivo, while SPI1 overexpression attenuated these effects.
CONCLUSIONS: This study demonstrated pro-metastatic mechanisms of transcription factor SPI1/FTL axis in OC and suggested it as a potential target for treating OC metastasis.
RESEARCH DESIGN AND METHODS: Bioinformatics methods were utilized to analyze FTL. Quantitative real-time polymerase chain reaction, western blot, and immunohistochemistry were employed for expression detection, and cell counting kit- 8, and transwell assays were for cell biological functions assessment. Extracellular acidification rate, oxygen consumption rate, and glycolytic metabolite contents were measured. Dual-luciferase and chromatin immunoprecipitation assay validated binding relationship. Xenografted tumor models in nude mice verified the role of FTL in vivo.
RESULTS: Cell function experiments revealed that FTL facilitated proliferation, migration, and invasion of OC cells. Rescue experiments unveiled that 2-Deoxy-D-glucose attenuated stimulation on OC cell metastasis and glycolysis by FTL overexpression. Salmonella pathogenicity island 1 (SPI1) up-regulated FTL expression to promote glycolysis and metastasis. FTL knockdown inhibited tumor growth and suppressed glycolysis and cell metastasis in vivo, while SPI1 overexpression attenuated these effects.
CONCLUSIONS: This study demonstrated pro-metastatic mechanisms of transcription factor SPI1/FTL axis in OC and suggested it as a potential target for treating OC metastasis.