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Fig. 3 | Biomarker Research

Fig. 3

From: Mechanisms of tRNA-derived fragments and tRNA halves in cancer treatment resistance

Fig. 3

tRF-Leu-CAG, ts-101, ts-46, and ts-47 are involved in drug resistance of lung cancer cells. Knockdown of tRF-Leu-CAG downregulates AURKA. AURKA overexpression induces gefitinib resistance by downregulating p53. The AURKA/NF-ĸB pathway is related to radio-resistance. ts-46 is associated with excessive activation of ILK, integrin, and mTOR signaling. Both ts-46 and ts-101 are correlated with the inhibition of PTEN signaling. RNA silencing of ILK enhances cisplatin sensitivity by regulating p-GSK3β, p-AKT, AP-1, β-catenin, cyclin D1, and MMP-9. Integrin activates Akt, which determines resistance to cisplatin. Integrin mediates EGFR-TKIs resistance through EMT, the KRAS-RalB-NF-κB pathway, and the Src/Akt pathway. Integrin/Src/Akt in NSCLC cells confers resistance to cixutumumab. PI3K/AKT/mTOR signaling promotes chemoresistance. ts-46 and ts-47 can affect the p53 pathway, which mediates cisplatin resistance in NSCLC

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