Recent research has uncovered that a long non-coding RNA known as FTX plays a significant role in the development of colorectal cancer (CRC) by promoting key metabolic pathways associated with tumor growth. The study revealed that lncRNA FTX is significantly upregulated in both cancer tissues and serum from patients suffering from CRC, indicating its potential as a biomarker for this prevalent cancer.
Colorectal cancer continues to rise in incidence, particularly in regions like China, prompting scientists to investigate molecular mechanisms that drive its progression. One of the metabolic alterations characteristic of cancer is known as the Warburg effect, where cancer cells preferentially utilize glycolysis to generate energy, even in the presence of oxygen. This phenomenon not only supports rapid cell proliferation but also contributes to the tumor’s aggressive nature.
The latest findings regarding lncRNA FTX suggest that it enhances aerobic glycolysis, cell proliferation, migration, and invasion in CRC cells. This is achieved through its interaction with miR-215-3p, a microRNA known to inhibit the oncoprotein YAP1. By sequestering miR-215-3p, FTX effectively reduces its capacity to repress YAP1, leading to increased glycolytic metabolism and subsequent tumor progression.
Additionally, the research demonstrated a negative correlation between the expression levels of lncRNA FTX and miR-215-3p in CRC patients. Experimental conditions confirmed that the knockdown of FTX reduced malignant behaviors in CRC cells while the overexpression of lncRNA FTX yielded opposite results, reinforcing its role as an oncogenic factor.
The collaborative research was conducted at The Third Affiliated Hospital of Zunyi Medical University, where blood samples were gathered from 25 advanced CRC patients alongside 32 healthy controls. Tumor growth effects were evaluated using various cell lines, including HT29 and HCT116, and xenograft models in nude mice, providing robust evidence of FTX's involvement in CRC metabolism and progression.
Notably, lncRNA FTX functions as a sponge for miR-215-3p within the CRC cellular milieu, enhancing glycolysis through the upregulation of YAP1, a key player in cancer metabolism. The findings present the lncRNA FTX-miR-215-3p-YAP1 regulatory axis as a novel mechanism driving CRC aggressiveness, positioning lncRNA FTX as a valuable target for therapeutic intervention.
The authors concluded that targeting this axis could yield promising results in treating colorectal cancer, underlining the significance of understanding metabolic pathways in cancer management. The study contributes vital insights in the quest to develop novel diagnostic and therapeutic strategies for CRC, highlighting the potential of lncRNA FTX as a therapeutic target.
