TABLE 1.

The exosomal factors involved in the chemoresistance of pancreatic cancer

Donor cells	Exosomal contents	Recipient cells	Functions	Mechanisms	Refs.
PANC‐1	EphA2	MIA PaCa‐2 and BxPC‐3	Induce chemoresistance of gemcitabine	Not yet clear	110
Panc1 and MiaPaCa2	MiR‐155	–	Promote gemcitabine resistance in vivo	Result in anti‐apoptotic activity by targeting TP53INP1	23
CAFs	Snail mRNA	Pancreatic cancer epithelial cells	Induce chemoresistance of gemcitabine in vitro	Not yet clear	24
BxR‐CSCs	MiR‐210	BxS and PANC‐1	Induce chemoresistance of gemcitabine	Trigger the mTOR signaling pathway.	86
TAM	MiR‐365	PDAC cells	Induce chemoresistance of gemcitabine in vitro	Upregulate the triphospho‐nucleotide pool in cancer cells and induce the enzyme cytidine deaminase	25
Gemcitabine‐treated PC cells	SOD2 and CAT transcripts	–	Induce chemoresistance of gemcitabine in vitro	Suppress basal and gemcitabine‐induced ROS production	102
Gemcitabine‐treated PC cells	MiR‐155	–	Induce chemoresistance of gemcitabine in vitro	Downregulate DCK	102
CAFs	MiR‐106b	–	Promote gemcitabine resistance	Target TP53INP1	76
GIPC‐depleted AsPC‐1 and PANC‐1 cells	ABCG2	–	Induce chemoresistance of gemcitabine in vitro	Serve as drug efflux transporter protein	22
BxPC‐3‐Gem cells	MMP14	BxPC‐3 and Mia‐PaCa‐2cells	Promote gemcitabine resistance	Increased cancer stemness and invasion properties	92

Abbreviations: EphA2, Ephrin type‐A receptor 2; TP53INP1, tumor protein 53‐induced nuclear protein 1; CAFs, cancer‐associated fibroblasts; CSCs, cancer stem cells; mTOR, mammalian target of rapamycin; TAM, tumor‐associated macrophages; PDAC, pancreatic ductal adenocarcinoma; PC, pancreatic cancer; ABCG2, The ATP‐binding cassette (ABC) superfamily G member 2; MMP14, matrix metalloproteinase 14.