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. 2021 May 19;40:174. doi: 10.1186/s13046-021-01974-y

Table 2.

Regulation of SE activity in 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 [186, 187]
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]

TNBC triple-negative breast cancer, PDAC pancreatic ductal adenocarcinoma, MCL mantle cell lymphoma, AKTi AKT inhibitor, IMiDs immunomodulatory drugs, BETi BET bromodomain inhibitors, GSI gamma-secretase inhibitor, NDME notch-dependent MYC enhancer, BDME BRD4-dependent MYC enhancer, RNA pol-II RNA polymerase-II, TSA trichostatin, ESC embryonic stem cell, CRC core transcription regulatory circuitry