Colorectal laterally spreading tumors show characteristic expression of cell polarity factors, including atypical protein kinase C λ/ι, E-cadherin, β-catenin and basement membrane component

Colorectal flat-type tumors include laterally spreading tumors (LSTs) and flat depressed-type tumors. The former of which shows a predominant lateral spreading growth rather than an invasive growth. The present study examined the morphological characteristics of LSTs, in comparison with polypoid- or flat depressed-type tumors, along with the expression of atypical protein kinase C (aPKC) lambda/iota, a pivotal cell polarity regulator, and the hallmarks of cell polarity, as well as with type IV collagen, beta-catenin and E-cadherin. In total, 37 flat-type (24 LSTs and I3 flat depressed-type tumors) and 20 polypoid-type colorectal tumors were examined. The LSTs were classified as 15 LST adenoma (LST-A) and nine LST cancer in adenoma (LST-CA). An immunohistochemical examination was performed on aPKC lambda/iota, type IV collagen, beta-catenin and E-cadherin. The LST-A and -CA showed a superficial replacing growth pattern, with expression of beta-catenin and E-cadherin in the basolateral membrane and type IV collagen along the basement membrane. In addition, 86.6% of LST-A and 55.6% of LST-CA showed aPKC lambda/iota expression of 1+ (weak to normal intensity staining in the cytoplasm compared with the normal epithelium). Furthermore, similar to 45% of the polypoid- type adenomas showed 2+ (moderate intensity staining in the cytoplasm, and/or nucleus) and 66.7% of the polypoid-type cancer in adenoma were 3+ (strong intensity staining in the cytoplasm and nucleus). A statistically significant positive correlation was observed between the expression of aPKC lambda/iota. and beta-catenin (r=0.842; P<0.001), or type IV collagen (r=0.823; P<0.001). The LSTs showed a unique growth pattern, different from the expanding growth pattern presented by a polypoid tumor and invasive cancer. The growth characteristics of LST appear to be caused by adequate coexpression of beta-catenin, type IV collagen and aPKC lambda/iota.