Table 4.

The Role of CAFs and ECM in the Tumor Microenvironment of Esophageal Cancer

Entry	Cancer Type	Finding	Effects on Tumors	Ref.
CAFs	ESCC	FAP+ CAFs-derived IL-6 promoted EMT and drug resistance, recruited FoxP3+ T cells, and induced M2 polarization of TAMs	Acceleration	[191–194]
	ESCC	uPA secreted by CAFs promotes ESCC progression through the PI3K/AKT and ERK pathways	Acceleration	[195]
	EC	The high expression of Twist1 in CAFs promotes the secretion of CXCL12 and EMT through the ERK/AKT pathway	Acceleration	[196,197]
	ESCC	HGF expressed by CAFs promotes progression and metastasis through the HGF/Met pathway	Acceleration	[198]
	ESCC	TGF-β1 expressed by CAFs promotes tumor progression through the TGF-β1/Smad pathway	Acceleration	[199,200]
ECM	ESCC	Cancer cells can produce cancer-derived type I collagen with a molecular weight different from CAFs-derived collagen and inhibit tumor growth	Acceleration	[216]
	ESCC	High matrix FN environment promotes movement and migration of ESCC cells	Acceleration	[217]
	ESCC	TNC can also improve cancer stem cell properties and promote EMT-like changes through the Akt/HIF1α axis	Acceleration	[219]
	ESCC	High expression of ESCC cell gene ADAM12-L can promote FAK activation and promote cancer cell metastasis and migration through FAK/JNK/c-Jun axis	Acceleration	[220]
	ESCC	Increased expression of LOX, LOXL4 and 5-LOX is associated with poor prognosis	Acceleration	[223–227]
	EAC	Elevated APE1 expression can induce ARF6 activity and up-regulate MMP-14, and up-regulation of MMP-14 can activate MMP-2 to mediate ECM degradation	Acceleration	[230,231]