LPIN3 promotes colorectal cancer growth by dampening intratumoral CD8+ T cell effector function.

Abstract

LPIN3 has emerged as a key factor in a variety of malignancies, although its precise role in colorectal cancer (CRC) remains unclear. By analyzing the data from The Cancer Genome Atlas, we discovered that the expression pattern of LPIN3 and the relevant makeup of the immune microenvironment were immensely diverse among tumors. LPIN3 is abundantly expressed in CRC and may enhance tumor growth by activating the β-catenin signaling pathway. In addition, we discovered that LPIN3 might reduce tumor antigen presentation signals, hence suppressing CD8⁺ T cell-mediated cytotoxicity. Furthermore, high expression of LPIN3 predicts decreased CD8⁺ T cell infiltration and effector function via bioinformatics analysis. Indeed, CD8⁺ T cell-mediated cytotoxicity as well as CD8⁺ T cell infiltration and activation in vivo were strengthened by LPIN3 knockdown. To sum up, our results highlight the part that LPIN3 plays in driving the progression of CRC by regulating β-catenin signaling and CD8⁺ T cell activity.