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Novel Oncogenes and Tumor Suppressor Genes in Hepatocellular Carcinoma: Carcinogenesis, Progression, and Therapeutic Targets Publisher Pubmed



Rahimifarsi N1 ; Bostanian F2 ; Shahbazi T3 ; Shamsinejad FS4 ; Bolideei M5 ; Mohseni P6 ; Zangooie A7, 8 ; Boustani F9 ; Shoorei H8, 9, 10
Authors
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Authors Affiliations
  1. 1. Department of Biology, University College of Nabi Akram, Tabriz, Iran
  2. 2. Institute of Biochemistry and Biophysics, University of Tehran
  3. 3. Neurosurgery Research Group (NRG), Razi Hospital, Tehran University of Medical Sciences, Tehran, Iran
  4. 4. Department of Biology, Shahed University, Tehran, Iran
  5. 5. Department of Respiratory and Critical Care Medicine, the Center for Biomedical Research, NHC Key Laboratory of Respiratory Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Sciences and Technology, Wuhan, China
  6. 6. Department of Pathobiology, Faculty of Veterinary Medicine, Shahid Bahonar University of Kerman, Kerman, Iran
  7. 7. Student Research Committee, Birjand University of Medical Sciences, Birjand, Iran
  8. 8. Department of Anatomical Sciences, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran
  9. 9. Clinical Research Development Unit of Tabriz Valiasr Hospital, Tabriz University of Medical Sciences, Tabriz, Iran
  10. 10. Cellular and Molecular Research Center, Birjand University of Medical Sciences, Birjand, Iran

Source: Gene Published:2025


Abstract

Hepatocellular carcinoma (HCC) is the primary malignancy affecting the liver and the leading cause of mortality among individuals with cirrhosis. This complex disease is associated with various risk factors, including environmental, pathological, and genetic influences, which dysregulate gene expression crucial for the cell cycle and cellular/molecular pathways. The disruption of the balance between tumor suppressors and proto-oncogenes amplifies the pathogenic cascade. Given its predilection for diseased or cirrhotic livers and late-stage diagnosis, HCC prognosis is typically poor. Current therapies offer limited benefits, with conventional non-specific cytotoxic agents exhibiting suboptimal efficacy. However, molecularly targeted therapies have emerged as a promising avenue, leveraging the strategic inhibition of carcinogenic molecules to provide heightened specificity and potency compared to cytotoxic chemotherapy. Several clinical trials have demonstrated promising outcomes in advanced HCC with targeted pharmacotherapies. Many genes have been implicated in HCC pathogenesis, underscoring the need to elucidate their molecular functions and roles. This has profound implications for early HCC prognostication via biomarkers and for identifying therapeutic targets to impede neoplastic progression. Notably, evidence highlights the pivotal roles of oncogenes and tumor suppressors in HCC pathophysiology. This discourse examines the potential involvement of ABL1, Annexins, FAK, FOX, and KIF as candidate oncogenes, contrasted with SORBS2, HPCAL1, PCDH10, PLAC8, and CXXC5 as plausible tumor suppressors. Their signaling cascades and relevance to HCC prognosis and progression are delineated to identify targets for improving HCC diagnosis, prognostication, and therapy. © 2025 Elsevier B.V.