Erlotinib might be a double‐edged sword in HCC

Dong, Jin-Zhong; Wang, Liping; Zhang, Sainan; Zou, Zhuolin; Lu, Mingqin

doi:10.1002/hep.27205

Cited by 2 publications

(1 citation statement)

References 6 publications

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“…Further study may investigate on whether β-defensin 1 expression may alter the sensitivity of hepatocellular carcinoma towards anthracyclines. EGFR signaling has been shown to play an important role in liver diseases 49 while Erlotinib, an EGFR inhibitor, was suggested to be an potential therapeutic agent 50 until the failure to demonstrate its efficacy in a phase III trial 51 .Although study on the combination of bevacizumab, an anti VEGFa antibody, and erlotinib has yielded promising results 52 , the clinical use of erlotinib in hepatocellular carcinoma has yet to be elucidated, especially, whether expression of β-defensin 1 could be a predictive biomarker for erlotinib warrant further investigation.…”

Section: Discussionmentioning

confidence: 99%

β-defensin 1 expression in HCV infected liver/liver cancer: an important role in protecting HCV progression and liver cancer development

Ling

Chen

Guo

et al. 2017

Sci Rep

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β-defensin family plays a role in host defense against viral infection, however its role in HCV infection is still unknown. In this study, we demonstrated that β-defensin 1 was significantly reduced in HCV-infected liver specimens. Treatment with interferon and ribavirin upregulated β-defensin-1, but not other β-defensin tested, with the extent and duration of upregulation associated with treatment response. We investigated β-defensin family expression in liver cancer in publicly available datasets and found that among all the β-defensins tested, only β-defensin 1 was significantly downregulated, suggesting β-defensin 1 plays a crucial role in liver cancer development. Further analysis identified E-cadherin as the top positive correlated gene, while hepatocyte growth factor-regulated tyrosine kinase substrate as the top negative correlated gene. Expression of two proteoglycans were also positively correlated with that of β-defensin 1. We have also identified small molecules as potential therapeutic agents to reverse β-defensin 1-associated gene signature. Furthermore, the downregulation of β-defensin 1 and E-cadherin, and upregulation of hepatocyte growth factor-regulated tyrosine kinase substrate, were further confirmed in liver cancer and adjacent normal tissue collected from in-house Chinese liver cancer patients. Together, our results suggest β-defensin 1 plays an important role in protecting HCV progression and liver cancer development.

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Section: Discussionmentioning

confidence: 99%