Apolipoprotein M promotes growth and inhibits apoptosis of colorectal cancer cells through upregulation of ribosomal protein S27a.

Colorectal cancer (CRC) is one of the frequent malignant tumors and has a high mortality-to-incidence ratio. Apolipoprotein M (ApoM), a lipoprotein superfamily member, is primarily bound to high-density lipoprotein (HDL) particles. Our previous studies opined that ApoM crucially modulates CRC progression, but its role in CRC has not been elucidated. Here, lentivirus infection technology was used to overexpress ApoM in Caco-2 cells. Cell growth, apoptosis as well as clone formation assays were performed to explore the biological influences of ApoM in Caco-2 cells. Differentially expressed genes were analyzed via GeneChip microarrays and Quantitative real-time PCR (qPCR) along with Western blotting were applied to verify the results. Ribosomal protein S27a (RPS27A) expression in CRC and tumor-adjacent tissues was detected by qPCR, and its correlation with clinicopathologic characteristics was explored. Our results showed that ApoM overexpression could promote Caco-2 cell proliferation and inhibit apoptosis. The microarray evaluation uncovered 2671 genes, which were differentially expressed, including RPS27A. The qPCR as well as the Western blotting data showed that ApoM overexpression significantly increased the expression of RPS27A. Moreover, RPS27A expression was remarkably higher in CRC tissues in contrast with the tumor-adjacent tissues and was positively correlated with the ApoM level in tumor tissues, and higher RPS27A expression was associated with smaller tumors and lower T stage. Functional recovery experiments indicated that knockdown of RPS27A counteracted the apoptosis inhibition and clone formation promotion induced by ApoM overexpression in Caco-2 cells. In conclusion, ApoM promotes CRC cell growth and inhibits apoptosis through upregulation of RPS27A.