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Table 4 Mutually dependent interactions with strong signals in PDAC dataset

From: CASTIN: a system for comprehensive analysis of cancer-stromal interactome

ligand

receptor

direction

signal strengtha

possible relevance for cancer-stromal interactions

SEMA3C

NRP1

C-S

101.5

SEMA3C induces growth and migration of endothelial cells [29], suggesting its angiogenic role; NRP1 also causes desmoplastic reaction in cancer [30].

WNT7B

GPC3

C-S

50

In hepatocellular carcinoma, GPC3 promotes cancer cell growth by Wnt signaling including WNT7B [53].

COL1A2

CD44

S-C

753

CD44 expressed in PDAC regulates its invasion [54].

COL1A1

CD44

S-C

668.4

CD44 expressed in PDAC regulates its invasion [54].

FN1

ITGA3

S-C

496.6

Not reported

COL1A2

ITGA2

S-C

348.4

α2β1 integrin-mediated adhesion on type I collagen promotes the malignant phenotype in PDAC [32].

COL1A1

ITGA2

S-C

341.1

α2β1 integrin-mediated adhesion on type I collagen promotes the malignant phenotype in PDAC [32].

FN1

ITGB6

S-C

180.8

Promotes breast cancer invasion [55].

SEMA4D

PLXNB1

S-C

63.4

Promotes cancer cell motility in PDAC [33].

SFRP1

FZD6

S-C

62

FZD6 overexpressed in several cancers [56]; SFRP1 is a Wnt antagonist.

IGF1

IGF1R

S-C

54.5

IGF1R induces PDAC growth and metastasis [57].

  1. aC-S: signal transduction from cancer cell-ligand to stromal receptor
  2. S-C: signal transduction from stromal ligand to cancer cell-receptor