Table 2.
The effect of targeting autophagy on glioblastoma survival in response to treatment (3-methyladenine, 3-MA; bafilomycin A1, BafA1; Beclin 1, BECN1; chloroquine, CQ; hydroxychloroquine, HCQ; suberoylanilide hydroxamic acid, SAHA; temozolomide, TMZ; tyrosine kinase inhibitor, TKI).
| treatment | autophagy modulator | treatment outcome | references |
|---|---|---|---|
| clinical trials | |||
| surgery + chemotherapy + radiotherapy | CQ | prolonged patient survival | [131,132] |
| surgery + chemotherapy + radiotherapy | HCQ | no survival advantage | [133] |
| recurrent glioblastoma following surgery + chemotherapy + radiotherapy | rapamycin/sirolimus (mTOR inhibitor) | no survival advantage | [134] |
| recurrent glioblastoma following surgery + chemotherapy + radiotherapy | Rapamycin/sirolimus (mTOR inhibitor) + Erlotinib (EGFR TKI) | no survival advantage | [135] |
| recurrent glioblastoma following surgery + chemotherapy + radiotherapy | everolimus (sirolimus derivative) + Gefitinib (EGFR TKI) | no survival advantage | [136] |
| mouse models | |||
| TMZ or SAHA | CQ | reduced tumour volume | [128] |
| ZD6474/vandetanib (multi TKI) | CQ | reduced subcutaneous tumour volume | [123] |
| cell culture | |||
| TMZ | 3-MA | promoted cell viability | [126] |
| BafA1 | enhanced cytotoxicity | ||
| imatinib (PDGFRα/β, c-abl, and c-kit TKI) | siATG5 / 3-MA | promoted cell viability | [124] |
| BafA1 | enhanced cytotoxicity | ||
| ZD6474/vandetanib (multi TKI) | shATG7 / shBECN1 / CQ / 3-MA | enhanced cytotoxicity | [123] |
| SAHA | rapamycin | improved cell viability | [129] |
| shLC3A / shBECN1 / shATG5 / BafA1 / CQ | enhanced cytotoxicity | ||
| SAHA | shATG7 | enhanced cytotoxicity | [130] |