From: Super-enhancers: a new frontier for epigenetic modifiers in cancer chemoresistance
Complex | Cancer | Resistant drugs | Induction methods | SE-associated genes | Mechanisms | References |
---|---|---|---|---|---|---|
H3K27ac | Glioblastoma | Temozolomide | 50 μM temozolomide | / | Transient resistant state | [183] |
Glioblastoma | Temozolomide | / | RFP/HDAC1 | Inhibit H3K27ac | [184] | |
Leukemia | / | / | Notch | Promote H3K27ac | ||
BRD4 | Breast cancer | AKTi | Stepwise method | SirT6, FOXO3a | BRD4/FOXO3a/CDK6 axis | [170] |
Melanoma | Vemurafenib | 1 μM vemurafenib | YAP/TAZ | Transcription addition mediated by YAP/TAZ through BRD4 | [171] | |
Myeloma | IMiDs | / | PP2A | Hyper pBRD4 | [172] | |
TNBC | BETi | Stepwise method | CK2, PP2A | pBRD4 increase MED1 recruitment | [173] | |
T cell leukemia | GSI | 1 μM GSI | NDME→BDME | Transition from NDME to BDME | [174] | |
Liposarcoma | Trabectedin | de novo | FUS-DDIT3 | Formation of CRC | [175] | |
PDAC | 5-FU | Stepwise method | HMGA2 | / | [176] | |
MCL | Ibrutinib, venetoclax and palbociclib | De novo | E3-ubiquitin ligase | / | [177] | |
CDK | B cell lymphoma | ABT-199 | 20 nM ABT-199 | BCL2 18q21 loss | Drug-tolerant “persister” state | [191] |
Leukemia cells | BETi | / | RNA pol-II, MYC | / | [193] | |
Anaplastic thyroid carcinoma | Doxorubicin | De novo | DNA damage repair | Downregulation of DNA damage repair | [192] | |
SEs formation | TNBC | Trametinib | / | RTKs/ERK | SEs de novo formation | [194] |
Hepatocellular carcinoma | Sorafenib, cisplatin | 5 μM/L sorafenib/cisplatin | Tex10 | Formation of ESC related SEs | [195] | |
ER+ breast cancer | Endocrine therapy | Doxycycline | ER-ligand-independent | Increased combination of ER and SEs | [196] | |
ER+ breast cancer | Endocrine therapy | Endocrine therapy | Endogenous cholesterol biosynthesis | Epigenetic reprogramming | [197] |