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Table 1 Observed effects due to MAP17 high expression in different cell lines and tumor types

From: Dr. Jekyll and Mr. Hyde: MAP17’s up-regulation, a crosspoint in cancer and inflammatory diseases

Concurring factors Tumor/ cell type Effect Treatment Ref.
SGLT1 upregulation Cervical, laryngeal Better survival Cisplatin + radiotherapy; Phloridzin, in vitro [36, 133]
γH2AX phosphorylation Laryngeal Better survival Cisplatin + radiotherapy [134]
ND Sarcoma Poor survival Cisplatin, oxaliplatin, gemcitabine, radiation [38, 133]
ND Breast N.D. Bortezomib, in vitro [31, 36, 39, 43]
ND Prostate N.D. N.D. [31, 36, 39]
SGLT2 increased activity N.D. Phloridzin, in vitro [74]
SLC34A2 downregulation A549 cells N.D. N.D. [53]
Notch pathway activation through MAP17-NUMB interaction T47D, HeLa, Calu3, sarcoma cells N.D. N.D. [41]
Reduced NFκB activation T47D, MDA-MB-231, sarcoma cells N.D. Bortezomib, in vitro [42, 43]
Reduced cell autophagy T47D, MDA-MB-231 cells N.D. Bortezomib, in vitro [43]
Decreased ERK1/2 phosphorylation T47D, MDA-MB-231 cells N.D. Bortezomib, in vitro [43]
Inhibition of p21, pRB dephosphorylation A375, T47D, Me180, HBL100 cells N.D. N.D. [32]
Increased ROS generation A375, T47D cells Increased sensitivity Antioxidants, in vitro [35, 39, 40]
Activation of AKT-PI3K RAT1 cells Increased sensitivity Antioxidants, in vitro [33]
p38α phosphorylation T47D cells, breast tumor Increased sensitivity Antioxidants, in vitro [39]