Probing cell metabolism on insulin like growth factor(IGF)‐1/tumor necrosis factor(TNF)‐α and chargeable polymers co‐immobilized conjugates

Abstract

Cell culturing on different synthetic biomaterials would reprogram cell metabolism for adaption to their living conditions because such alterations in cell metabolism were necessary for cellular functions on them. Here we used metabolomics to uncover metabolic changes when liver cells were cultured on insulin‐like growth factor (IGF)/tumor necrosis factor‐α (TNF‐α) and chargeable polymers co‐modified biomaterials with the aim to explain their modulating effects on cell metabolism. The results showed that cell metabolism on IGF‐1/TNF‐α co‐immobilized conjugates was significantly regulated according to their scatterings on the score plot of principal component analysis. Specifically, cell metabolisms were reprogrammed to the higher level of pyrimidine metabolism, β‐alanine metabolism, and pantothenate and CoA biosynthesis, and the lower level of methionine salvage pathway in order to promote cell growth on IGF/TNF‐α co‐modified surface. Furthermore, cell senescence on PSt‐PAAm‐IGF/TNF‐α surface was delayed through the regulation of branch amino acid metabolism and AMPK signal pathway. The research showed that metabolomics had great potential to uncover the molecular interaction between biomaterials and seeded cells, and provide the insights about cell metabolic reprogramming on IGF/TNF‐α co‐modified conjugates for cell growth.

Metabolomics profiling reveals differences in proliferation between tumorigenic and non-tumorigenic Madin-Darby canine kidney (MDCK) cells

“…3 ). Previous studies have also indicated that β-alanine may be associated with cell energy metabolism and proliferation ( Comerford et al, 2014 ; Li et al, 2018 ; You et al, 2021 ). The metabolic processing of tryptophan was notably increased in the MDCK-XF06 cell group.…”

Dihydropyrimidine dehydrogenase (DPYD) gene c.1627A>G A/G and G/G genotypes are risk factors for lymph node metastasis and distant metastasis of colorectal cancer

“…A common feature of metabolism in the cancer cells is the ability to acquire necessary nutrients from a frequently nutrient‐poor environment and utilize these nutrients to both maintain viability and build new biomass 48 . Some studies have shown that Pantothenate and CoA biosynthesis signaling pathway was significantly altered in tumor cells 49–51 . DPD is a key enzyme in the Pantothenate and CoA biosynthesis signaling pathway (https://www.genome.jp/pathway/ko00770%2BK00207).…”