| Literature DB >> 33669204 |
Mai-Huong Thi Ngo1,2, Han-Yin Jeng3, Yung-Che Kuo3, Josephine Diony Nanda1, Ageng Brahmadhi1, Thai-Yen Ling4, Te-Sheng Chang5,6, Yen-Hua Huang1,2,3,7,8,9,10,11.
Abstract
Insulin-like Growth Factor (IGF)/IGF-1 Receptor (IGF-1R) signaling is known to regulate stem cell pluripotency and differentiation to trigger cell proliferation, organ development, and tissue regeneration during embryonic development. Unbalanced IGF/IGF-1R signaling can promote cancer cell proliferation and activate cancer reprogramming in tumor tissues, especially in the liver. Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related death, with a high incidence and mortality rate in Asia. Most patients with advanced HCC develop tyrosine kinase inhibitor (TKI)-refractoriness after receiving TKI treatment. Dysregulation of IGF/IGF-1R signaling in HCC may activate expression of cancer stemness that leads to TKI refractoriness and tumor recurrence. In this review, we summarize the evidence for dysregulated IGF/IGF-1R signaling especially in hepatitis B virus (HBV)-associated HCC. The regulation of cancer stemness expression and drug resistance will be highlighted. Current clinical treatments and potential therapies targeting IGF/IGF-1R signaling for the treatment of HCC will be discussed.Entities:
Keywords: IGFs inhibitor; cancer stemness; insulin-like growth factor; liver cancer; targeting drug resistance
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Year: 2021 PMID： 33669204 PMCID： PMC7919800 DOI： 10.3390/ijms22041931
Source DB: PubMed Journal: Int J Mol Sci ISSN： 1422-0067 Impact factor: 5.923