Abstract
Identification of changes of phospholipid (PL) composition occurring during colorectal cancer (CRC) development may help us to better understand their roles in CRC cells. Here, we used LC-MS/MS-based PL profiling of cell lines derived from normal colon mucosa, or isolated at distinct stages of CRC development, in order to study alterations of PL species potentially linked with cell transformation. We found that a detailed evaluation of phosphatidylinositol (PI) and phosphatidylserine (PS) classes allowed us to cluster the studied epithelial cell lines according to their origin: i) cells originally derived from normal colon tissue (NCM460, FHC); ii) cell lines derived from colon adenoma or less advanced differentiating adenocarcinoma cells (AA/C1, HT-29); or, iii) cells obtained by in vitro transformation of adenoma cells and advanced colon adenocarcinoma cells (HCT-116, AA/C1/SB10, SW480, SW620). Although we tentatively identified several PS and PI species contributing to cell line clustering, full PI and PS profiles appeared to be a key to the successful cell line discrimination. In parallel, we compared PL composition of primary epithelial (EpCAM-positive) cells, isolated from tumor and adjacent non-tumor tissues of colon cancer patients, with PL profiles of cell lines derived from normal colon mucosa (NCM460) and from colon adenocarcinoma (HCT-116, SW480) cells, respectively. In general, higher total levels of all PL classes were observed in tumor cells. The overall PL profiles of the cell lines, when compared with the respective patient-derived cells, exhibited similarities. Nevertheless, there were also some notable differences in levels of individual PL species. This indicated that epithelial cell lines, derived either from normal colon tissue or from CRC cells, could be employed as models for functional lipidomic analyses of colon cells, albeit with some caution. The biological significance of the observed PL deregulation, or their potential links with specific CRC stages, deserve further investigation.
Highlights
The colorectal cancer (CRC) development is a complex multi-step process, which involves a gradual progression from adenomatous polyp to adenoma, and to malignant carcinoma [1]
The colon adenoma-carcinoma sequence has been suggested to be accompanied with alterations of lipid profile(s) and/or lipid metabolism, which may contribute to tumor progression, as well as to cancer cell heterogeneity [2]
These included: NCM460 cells, derived from normal adult colon mucosa; FHC cells derived from normal fetal human colon; cell lines derived from colon adenoma, RG/C2 and AA/C1 cells, as well as in vitro transformed variant of AA/C1 cell line, AA/C1/SB10 cells; and cell lines derived from colon adenocarcinoma— HT-29, HCT-116, SW480, as well as SW620 cell line, which has been derived from a lymph node metastasis of the same patient as SW480 cell line
Summary
The colorectal cancer (CRC) development is a complex multi-step process, which involves a gradual progression from adenomatous polyp to adenoma, and to malignant carcinoma [1]. The colon adenoma-carcinoma sequence has been suggested to be accompanied with alterations of lipid profile(s) and/or lipid metabolism, which may contribute to tumor progression, as well as to cancer cell heterogeneity [2]. This deregulation of lipid metabolism can have a major impact on both structure and function of cellular membranes, as well as on the lipid metabolism in cancer cells. CRC development seems to be associated with changes FA profiles both in tumor tissue and in patient’s serum
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