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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2017.1
- 수록면
- 9 - 18 (10page)
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Purpose: Rearrangement of the proto-oncogene rearranged during transfection (RET) has been newly identified potential driver mutation in lung adenocarcinoma. Clinically available tyrosine kinase inhibitors (TKIs) target RET kinase activity, which suggests that patients with RET fusion genes may be treatable with a kinase inhibitor. Nevertheless, the mechanisms of resistance to these agents remain largely unknown. Thus, the present study aimed to determine whether epidermal growth factor (EGF) and hepatocytegrowth factor (HGF) trigger RET inhibitor resistance in LC-2/ad cells with CCDC6-RET fusion genes.
Materials and Methods: The effects of EGF and HGF on the susceptibility of a CCDC6-RET lung cancer cell line to RET inhibitors (sunitinib, E7080, vandetanib, and sorafenib) were examined.
Results: CCDC6-RET lung cancer cells were highly sensitive to RET inhibitors. EGF activated epidermal growth factor receptor (EGFR) and triggered resistance to sunitinib, E7080, vandetanib, and sorafenib by transducing bypass survival signaling through ERK and AKT. Reversible EGFR-TKI (gefitinib) resensitized cancer cells to RET inhibitors, even in the presence of EGF. Endothelialcells, which are known to produce EGF, decreased the sensitivity of CCDC6-RET lung cancer cells to RET inhibitors, an effect that was inhibited by EGFR small interfering RNA (siRNA), anti-EGFR antibody (cetuximab), and EGFR-TKI (Iressa). HGF had relatively little effect on the sensitivity to RET inhibitors.
Conclusion: EGF could trigger resistance to RET inhibition in CCDC6-RET lung cancer cells, and endothelial cells may confer resistanceto RET inhibitors by EGF. E7080 and other RET inhibitors may provide therapeutic benefits in the treatment of RET-positivelung cancer patients.
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참고문헌 (24)
참고문헌 신청
Lynch TJ / 2004 / Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib / N Engl J Med 350:2129~2139
Bergethon K / 2012 / ROS1 rearrangements define a unique molecular class of lung cancers / J Clin Oncol 30:863~870
Tanizaki J / 2012 / Activation of HER family signaling as a mechanism of acquired resistance to ALK inhibitors in EML4-ALK-positive non-small cell lung cancer / Clin Cancer Res 18:6219~6226
Eng C / 1999 / RET proto-oncogene in the development of human cancer / J Clin Oncol 17:380~393
Wang R / 2012 / RET fusions define a unique molecular and clinicopathologic subtype of non-smallcell lung cancer / J Clin Oncol 30:4352~4359
Bergethon K / 2012 / ROS1 rearrangements define a unique molecular class of lung cancers / J Clin Oncol 30:863~870
Tanizaki J / 2012 / Activation of HER family signaling as a mechanism of acquired resistance to ALK inhibitors in EML4-ALK-positive non-small cell lung cancer / Clin Cancer Res 18:6219~6226
Eng C / 1999 / RET proto-oncogene in the development of human cancer / J Clin Oncol 17:380~393
Wang R / 2012 / RET fusions define a unique molecular and clinicopathologic subtype of non-smallcell lung cancer / J Clin Oncol 30:4352~4359
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