<p>Malignant tumors, as one of the leading causes of mortality, pose great threats to global public health. Serine/Arginine-rich Splicing Factor 7 (SRSF7), a core splicing regulatory protein of the SRSF family, plays a crucial role in maintaining RNA stability, facilitating alternative splicing, and assisting RNA nuclear export. It also exhibits significantly aberrant expression among various cancers, including lung, colorectal, liver, and oral cancer. This review examines the molecular mechanisms of SRSF7 in tumorigenesis, with a focus on its role in the epigenetic reprogramming of related tumors. Specifically, it explores the abnormal regulation of the cell cycle, the regulation of non-coding RNA, the control of RNA methylation, and the reprogramming of glucose metabolism. Additionally, this review examines the role of SRSF7 in the tumor immune microenvironment through alternative splicing and immune evasion through the immune checkpoint PD-1. It also highlights the role of SRSF family members in tumor resistance, illustrating how alternative splicing contributes to tumor chemoresistance. Although SRSF7 shows significant promise in tumor intervention therapies, more experimental and clinical studies are still needed to evaluate its clinical application. This review enhances our understanding of the molecular landscape of SRSF7 in tumorigenesis with great potential to become a key node in tumor-targeted therapy and companion diagnostics, driving translational potential from mechanisms to clinical applications.</p>

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Multidimensional regulatory roles and therapeutic applications of SRSF7 in cancer

  • Yuan Li,
  • Huimeng Gao,
  • Xuanyu Zhang,
  • Fuli Sun,
  • Yan Guo,
  • Xue Qiao

摘要

Malignant tumors, as one of the leading causes of mortality, pose great threats to global public health. Serine/Arginine-rich Splicing Factor 7 (SRSF7), a core splicing regulatory protein of the SRSF family, plays a crucial role in maintaining RNA stability, facilitating alternative splicing, and assisting RNA nuclear export. It also exhibits significantly aberrant expression among various cancers, including lung, colorectal, liver, and oral cancer. This review examines the molecular mechanisms of SRSF7 in tumorigenesis, with a focus on its role in the epigenetic reprogramming of related tumors. Specifically, it explores the abnormal regulation of the cell cycle, the regulation of non-coding RNA, the control of RNA methylation, and the reprogramming of glucose metabolism. Additionally, this review examines the role of SRSF7 in the tumor immune microenvironment through alternative splicing and immune evasion through the immune checkpoint PD-1. It also highlights the role of SRSF family members in tumor resistance, illustrating how alternative splicing contributes to tumor chemoresistance. Although SRSF7 shows significant promise in tumor intervention therapies, more experimental and clinical studies are still needed to evaluate its clinical application. This review enhances our understanding of the molecular landscape of SRSF7 in tumorigenesis with great potential to become a key node in tumor-targeted therapy and companion diagnostics, driving translational potential from mechanisms to clinical applications.