<p>Colorectal cancer (CRC) remains a major global health burden and a leading cause of cancer-related morbidity and mortality. It ranks as the third most commonly diagnosed malignancy and the second leading cause of cancer-related deaths worldwide. These statistics underscore the urgent need for improved diagnostic, prognostic, and therapeutic strategies to combat the disease. The development of CRC is driven by a combination of genetic predisposition, environmental exposures, and lifestyle-related factors. Major risk factors include a family history of CRC, unhealthy diet, smoking, excessive alcohol consumption, and chronic intestinal inflammation. Effective CRC management relies heavily on early detection through colonoscopy, imaging modalities, and biomarker-based analyses. Standard treatment options include surgery, chemotherapy, radiotherapy, and targeted therapy, selected according to disease stage and patient condition. Emerging evidence identifies long non-coding RNAs (lncRNAs) as pivotal regulators of CRC progression, modulating gene expression and tumor biology. Among these, the lncRNA colon cancer-associated transcript 2 (CCAT2) has recently been recognized as a critical driver of CRC growth and metastasis. CCAT2 regulates gene expression and preserves chromosomal stability by modulating key oncogenic signaling pathways, including Wnt/β-catenin and MYC. Preliminary studies propose CCAT2 as a potential therapeutic target in CRC; however, further investigation is required to validate its feasibility, especially regarding delivery strategies and molecular specificity. This review provides a comprehensive overview of lncRNA CCAT2 in CRC development, emphasizing its underlying molecular mechanisms. It further discusses potential of CCAT2 as a diagnostic and prognostic biomarker, highlighting its relevance for future clinical application.</p>

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The CCAT2 enigma: pioneering insights into colorectal cancer pathophysiology and therapeutic innovation

  • Maryam Fathollahzadeh,
  • Ahmad Ghorbani Vanan,
  • Nafise Mohammadmoradi,
  • Farid Ghorbaninezhad,
  • Pooya Eini,
  • Mohammad Amin Tofighi Zavareh,
  • Yasamin Rahmani,
  • Samaneh Rostami,
  • Safa Tahmasebi,
  • Elham Safarzadeh

摘要

Colorectal cancer (CRC) remains a major global health burden and a leading cause of cancer-related morbidity and mortality. It ranks as the third most commonly diagnosed malignancy and the second leading cause of cancer-related deaths worldwide. These statistics underscore the urgent need for improved diagnostic, prognostic, and therapeutic strategies to combat the disease. The development of CRC is driven by a combination of genetic predisposition, environmental exposures, and lifestyle-related factors. Major risk factors include a family history of CRC, unhealthy diet, smoking, excessive alcohol consumption, and chronic intestinal inflammation. Effective CRC management relies heavily on early detection through colonoscopy, imaging modalities, and biomarker-based analyses. Standard treatment options include surgery, chemotherapy, radiotherapy, and targeted therapy, selected according to disease stage and patient condition. Emerging evidence identifies long non-coding RNAs (lncRNAs) as pivotal regulators of CRC progression, modulating gene expression and tumor biology. Among these, the lncRNA colon cancer-associated transcript 2 (CCAT2) has recently been recognized as a critical driver of CRC growth and metastasis. CCAT2 regulates gene expression and preserves chromosomal stability by modulating key oncogenic signaling pathways, including Wnt/β-catenin and MYC. Preliminary studies propose CCAT2 as a potential therapeutic target in CRC; however, further investigation is required to validate its feasibility, especially regarding delivery strategies and molecular specificity. This review provides a comprehensive overview of lncRNA CCAT2 in CRC development, emphasizing its underlying molecular mechanisms. It further discusses potential of CCAT2 as a diagnostic and prognostic biomarker, highlighting its relevance for future clinical application.