80 for tcPTC has confirmed 4 putative miRNA regulatory pairs: hsamiR-146b-5p with PHKB and IRAK1; hsa-miR-874-3p with ITGB4 within cPTC samples (Table 1, Figure 3).
According to our integrative analysis we report four new regulations in PTC: hsa-miR-146b-5p regulating PHKB (phosphorylase kinase, beta), hsa-miR-146b-5p regulating IRAK1 (interleukin-1 receptor-associated kinase 1) and hsamiR-874-3p regulating ITGB4 (integrin, beta 4) in cPTC samples, and hsa-miR-152-3p regulating TGFA (transforming growth factor, alpha) in fvPTC samples.
Putative regulation of ITGB4 expression by hsamiR-874-3p was observed in cPTC samples and may be also present in fvPTC variant (Figure 3).
Four putative miRNA regulatory pairs were discovered: hsa-miR-146b-5p with PHKB and IRAK1, hsa-miR-874-3p with ITGB4 characteristic for cPTC samples, and hsa-miR-152-3p with TGFA characteristic for fvPTC samples.
Pairs hsa-miR-146b-5p with PHKB (a), hsa-miR-146b-5p with IRAKI, (b) and hsa-miR-874-3p with ITGB4 (c) were selected from best inverse Spearman's correlations (below -0.
001 survival CASP1, CBR1, CRABP2, CSTB, EEF1A1, EIF6, ENO1, FLNA, GAPDH, HMGB2, HSP90AA1, HSP90AB1, HSPA8, HSPB1, ITGB4
, KRT14, KRT6A, KRT8, LMNA, NDRG1, PDCD6IP, PRDX2, S100A8, S100A9, SFN, TF, TPM1, TRIM29, TUBB, TUBB3, TXN, VCL, YWHAZ Cancer ANXA2, ENO1, 11 < .
Differential expression of pyloric atresia in junctional epidermolysis bullosa with ITGB4
mutations suggests that pyloric atresia is due to factors other than the mutations and not predictive of a poor outcome: three novel mutations and a review of the literature.
Genomics of Epidermolysis Bullosa EB Type Level of Blistering Genes Simplex Basal cell layer KRT5, KRT14 Hemidesmosomal Basal cell/lamina BPAG2, ITGB4
, ITGA6 lucida interface (PLEC1 with muscular dystrophy) Junctional Lamina lucida LAMA3, LAMB3, LAMC2 Dystrophic Sublamina densa COL7A1 Source: Dr.
74) Eleven genes--COL1A2, COL6A1 (collagen), tPA, MMP9 (protease), CDH3, L1CAM, ITGB4, PLXNA3/PLXN3, KRT14/K14 (cell adhesion or cell surface molecule), SEMA3C (semaphorin), and CXCL10/INP10 (chemokine)--were overexpressed in MPM.
In the comparative study with normal cells quoted above, (74) SEMA3C, ITGB4, CDH3, and COL6A1 were highly expressed in the epithelioid MPM subtype; L1CAM, K14, and INP10 were overexpressed in the mixed MPM subtype; and MMP9 and PLXN3 were overexpressed in the sarcomatoid MPM subtype.
L1CAM, INP10, P-cadherin, tPA and ITGB4 over-expression in malignant pleural mesotheliomas revealed by combined use of cDNA and tissue microarray.