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

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

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]

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