Table 5.
Deregulated miRNAs and relation to OS in liver cancer.
| miRNA | Evidence | Target Gene/Pathway | (Patho)Mechanism | References | |||
|---|---|---|---|---|---|---|---|
| In Vitro | In Vivo | In Situ | In Silico | ||||
| 26↓1 | ✓ | ✓ | EZH2 ↑ | Sequestration of miR-26 from its target EZH2, which released the suppression on EZH2, and thereby led to EZH2 overexpression in gastric cancer | [142] | ||
| 29b↓2 | ✓ | ✓ | TET1 ↓ | Feedback of miRNA-29-TET1 downregulation in HCC development suggesting a potential target in identification of the prognosis and application of cancer therapy for HCC patients | [144] | ||
| 494↑2 | ✓ | ✓ | TET1 ↓ | miR-494 inhibition or enforced TET1 expression is able to restore invasion-suppressor miRNAs and inhibit miR-494-mediated HCC cell invasion | [145] | ||
| 520b↓2 | ✓ | TET1 ↓ | Depresses proliferation of liver cancer cells through targeting 3’UTR of TET1 mRNA | [146] | |||
| 17-92 cluster↓1 | ✓ | E2F family ↑ | ROS-mediated oxidative DNA damage correlates with over-expression of miR-92–playing a role in both the apoptotic process and in cellular proliferation pathways | [147] | |||
Relation to oxidative stress: 1: yes, 2: no, 3: not mentioned. Abbreviations: E2F = E2F transcription factor family, EZH2 = Enhancer of zeste homolog 2, TET1 = Ten-eleven translocation methylcytosine dioxygenase 1, ↓ = downregulation/reduction, ↑ = upregulation/increase.