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Table 2 Biological mechanisms between lipid metabolism and EC

From: Etiological relationship between lipid metabolism and endometrial carcinoma

Lipid Type

Mechanism or Pathway

HDL-C

HDL→ApoA I→T-cell→MNC→TNF-α, IL-1β↓→Inflammatory factors

HDL→ApoA I→M2→M1↑→Antitumor

LDL-C

LDL→LDLR→ROS→PI3K/MAP↑→Carcinogenic effect

LDL→LDLR→ROS→NF-κB→HER2 PGF RAS EGFR↑→Genetic mutations

ROS→LDL-C→OX-LDL→CD36 LOX-1↑→Growth and metastasis

TC

TC→27HC→IL-6 TNF↑→Inflammatory factors

TC→27HC→ER↑→Uterine epithelial cell proliferation

TC→27HC→LXR↑→Growth and metastasis

TG

TG→SHBG + E→E↑→Angiogenesis and proliferation

TG→PPARα↑→Carcinogenic effect

TG→IHF→IR-A IGF-1R→PI3K/AKT ERK MAPK↑→Malignant phenotype

  1. MNC, mononuclear cell; M1, macrophage 1; M2, macrophage 2; ROS, reactive oxygen species; LOX-1, lectin-like oxidized LDL receptor-1; 27HC, 27-hydroxycholesterol; LXR, liver X receptor; E, estrogen; ER, estrogen receptor; SHBG, sex hormone-binding globulin; IHF, impaired hepatic function; IR-A, insulin receptor-A; IGF-1R, insulin-like growth factor 1 receptor; “↑” represents positive regulation; “↓” represents negative regulation