IGF2BP1 accelerates the aerobic glycolysis to boost its immune escape in hepatocellular carcinoma microenvironment.

ABSTRACT:

Introduction

Energy metabolism abnormity emerges as a crucial factor that facilitates tumorigenesis by accelerating aerobic glycolysis. However, the function of N⁶-methyladenosine (m⁶A) on hepatocellular carcinoma (HCC) aerobic glycolysis and immune escape is still unclear. Here, this investigation was intended to elucidate the regulation of m⁶A 'reader' IGF2BP1 involved in HCC aerobic glycolysis and immune escape.

Methods

The aerobic glycolysis was tested by glucose uptake, lactate, ATP generation and ECAR. The CD8⁺ T cell-mediated killing effect was tested by cytotoxicity, IFN-γ and granzyme B. The molecular interaction was confirmed by luciferase reporter assay, immunoprecipitation assay and chromatin immunoprecipitation (ChIP)-

SUBMITTER: Ye X 

PROVIDER: S-EPMC11599169 | biostudies-literature | 2024

REPOSITORIES: biostudies-literature