Key factor or pathway | Agent | Major mechanism | Tumor type | Year and Reference |
---|---|---|---|---|
EGFR | Erlotinib | - | Locally advanced ESCC | 2020 [179] |
EGFR-ERK | Cetuximab | G2/M cycle arrest and DNA repair delay | ECA109 and TE-13 cell lines | 2023 [180] |
EGFR | Icotinib | - | Older adults with unresectable ESCC | 2020 [108] |
EGFR | Nimotuzumab + cetuximab | - | Locally advanced ESCC | 2019 [106] |
VEGF, HIF-1α | 2-Methoxyestradiol | Inhibited proliferation of ESCC cells | ECA109 cell line | 2019 [116] |
VEGF, PD-1 | Camrelizumab + apatinib | Anti-angiogenic | Advanced ESCC | 2020 [123] |
c-Met | BPI-9016Â M | Inhibited the ATM- and ATR-dependent DNA damage HR recombination repair | ECA109 cell lines | 2021 [74] |
c-Met | Foretinib | Inhibited proliferation and prompted the G2/M arrest of ESCC cells, delays the DNA damage repair | ECA109 and TE-13 cell lines | 2017 [137] |
Wnt/β-catenin | RASSF10 | Inhibited epithelium-mesenchymal transition | ESCC patients and TE-10, ECA-109 and KYSE-150 cell lines | 2022 [140] |
PI3K/Akt/mTOR | FAM135B | Promotes cell cycle redistribution | KYSE150, ECA109, TE-13, TE-10, and TE-1 cell lines | 2021 [181] |
PI3K/Akt/mTOR | UHRF1 | Increased ESCC cell apoptosis | The human ESCC, ECA109, and TE-1 cell lines | 2021 [132] |