Table 4 Role of PI3K/AKT pathway in pharyngeal squamous cell carcinoma
From: Role of PI3K/AKT pathway in squamous cell carcinoma with an especial focus on head and neck cancers
Type of diseases | Samples | Cell lines | Drug/phytotherapy | Dose range | Target | Pathway | Function | Refs. |
|---|---|---|---|---|---|---|---|---|
Hypopharyngeal Squamous Cell Carcinoma (HPSCC) | HPSCC (n = 55) | FaDu | GDC-0980, Refametinib | 0–5 µM, 0-20 µM | cyclin D1, p27, pRb, p-PKCζ, p-Integrin β1 | PI3K/AKT, MAPK/ERK | GDC-0980 and refametinib via inhibiting the PI3K/AKT and MAPK/ERK pathways can suppress HPSCC cell proliferation, migration, and arrest cell cycle | [60] |
HPSCC | 16 pairs of HPSCC and nearby non-cancerous tissues | FaDu | – | – | calcium-binding protein A11, S100A11, EGFR, CD44, MMP2/9, Bcl-2 | PI3K/AKT, mTOR | S100A11 via the PI3K/AKT pathway participates in the migration, carcinogenesis and protection of HPSCC from cell death induced by 5-Fu | [63] |
HPSCC | 12 pairs of HPSCC and adjacent normal tissues, male BALB/cAnN.Cg nude mice | FaDu | NVP-BEZ235, Cisplatin | 50Â nM, 2000Â nM | 4E-PB1, Caspase 3, PARP | PI3K/AKT, mTOR | NVP-BEZ235 when combined with cisplatin could synergistically inhibit HPSCC cell proliferation and arrest cell cycle at G2/M phase via the PI3K/AKT/mTOR pathway | [61] |
HPSCC | – | FaDu | – | – | JARID1B, K10, Flag, H3K4me3, β-catenin | SHIP1/AKT | JARID1B via the SHIP1/AKT pathway could improve HPSCC cell differentiation and suppress proliferation | [62] |
HPSCC | 56 pairs of HPSCC and adjacent normal tissues, male nude mice | FaDu | – | – | Argonaute 2 (AGO2), p53, Caspase-3, FAK | PI3K/AKT | AGO2 via the FAK/PI3K/AKT pathway could increase tumor growth, proliferation, migration, and invasion of HPSCC cell | [64] |
HPSCC | – | FaDu, 293 T | EGFRmAb–AuNPs | 20 mM | Bcl-2, Bax, Caspase-3/9 | PI3K/AKT, mTOR | Photothermal treatment with EGFRmAb–AuNPs via the PI3K/AKT/mTOR pathway and DNA destruction enhances apoptosis in HPSCC cells | [65] |
Oropharyngeal Squamous Cell Carcinoma (OPSCC) | OPSCC (n = 116) | – | – | – | PTEN | AKT | HPV could activate the PI3K/AKT pathway and increase levels of pAKT (Ser473) and PTEN in OPSCC | [66] |
OPSCC | OPSCC (n = 121) | – | – | – | EGFR, PTEN | AKT | Because of HPV, level of PTEN, EGFR and pAKT, could be different between oropharyngeal and oral cavity squamous cell carcinoma | [67] |
Pharyngeal Squamous Cell Carcinoma (PSCC) | – | NHOK, FaDu | Adenosine | 0–3 mM | Bax, Bcl-2, caspase-3/9 | PI3K/AKT, mTOR | Adenosine via the PI3K/AKT/mTOR pathway and activating caspase-3/9 could induce mitochondrial intrinsic apoptosis in PSCC cells | [68] |