@Article{biocell.2023.025048,
AUTHOR = {LIJUN DU, KAIKAI DOU, NIANHAI LIANG, JIANMIN SUN, RU BAI},
TITLE = {MiR-194-5p suppresses the warburg effect in ovarian cancer cells through the IGF1R/PI3K/AKT axis},
JOURNAL = {BIOCELL},
VOLUME = {47},
YEAR = {2023},
NUMBER = {3},
PAGES = {547--554},
URL = {http://www.techscience.com/biocell/v47n3/51083},
ISSN = {1667-5746},
ABSTRACT = {<b>Background:</b> The Warburg effect is considered as a hallmark of various types of cancers, while the regulatory
mechanism is poorly understood. Our previous study demonstrated that miR-194-5p directly targets and regulates
insulin-like growth factor1 receptor (IGF1R). In this study, we aimed to investigate the role of miR-194-5p in the
regulation of the Warburg effect in ovarian cancer cells. <b>Methods:</b> The stable ovarian cell lines with miR-194-5p
overexpression or silencing IGF1R expression were established by lentivirus infection. ATP generation, glucose uptake,
lactate production and extracellular acidification rate (ECAR) assay were used to analyze the effects of aerobic glycolysis
in ovarian cancer cells. Gene expression was analyzed by quantitative polymerase chain reaction (qPCR) and western
blot. Immunohistochemistry assays were performed to assess the expression of the IGF1R protein in ovarian cancer
tissues. <b>Results:</b> Overexpression of miR-194-5p or silencing IGF1R expression in ovarian cancer cells decreases ATP
generation, glucose uptake, lactate production, and ECAR and inhibits both the mRNA and protein expression of
PKM2, LDHA, GLUT1, and GLUT3. While the knockdown of miR-194-5p expression led to opposite results.
Overexpression of miR-194-5p or silencing IGF1R expression suppressed the phosphatidylinositol-3-kinase/protein
kinase B (PI3K/AKT) pathway, whose activation can sustain aerobic glycolysis in cancer cells, and the knockdown of
miR-194-5p expression promoted the activation of the PI3K/AKT pathway. <b>Conclusion:</b> Our results suggest that miR-
194-5p can inhibit the Warburg effect by negative regulation of IGF1R and further repression of the PI3K/AKT
pathway, which provides a theoretical basis for further test of miR-194-5p as a target in the treatment of ovarian cancer.},
DOI = {10.32604/biocell.2023.025048}
}