Abstract

This research aimed to analyze the biocompatibility and growth behavior of human immunodeficiency virus (HIV)-associated colorectal cancer (CRC) cells on a polylactic acid/polyglycolic acid (PLA-PCL) composite nanofiber scaffold (CNS) using proteomic analysis. The PLA-PCL CNS was prepared using a gel extraction phase separation (GEPS) method in a dioxane/ethanol solvent system, and the effects of gel temperature, PLA-PCL mass ratio (MR), solvent-to-polymer MR on the structure and properties of the PLA-PCL CNS were analyzed. Subsequently, Lappaol F (LAF) was incorporated into the PLA-PCL CNS using electrospinning (ES) technology, and tissue specimens were obtained from HIV-associated CRC patients to investigate the impacts of LAF-PLA-PCL CNS on the growth behavior of HIV-associated CRC cells through mass spectrometry and bioinformatics analysis. Field emission scanning electron microscopy (FE-SEM) revealed that the CNS could be obtained at gel temperatures between −20 °C and −10 °C, PLA-to-PCL MRs of 1:1, 3:2, 7:3, and ethanol content of 5%–15%. X-ray diffraction (XRD) and differential scanning calorimetry (DSC) showed that the PLA-to-PCL MR of 70:30 exhibited compatibility and crystallinity of the PLA-PCL CNS, while the porosity increased with an increase in PCL content. Fourier-transform infrared spectroscopy (FTIR) analysis indicated a good biological activity of the PLA-PCL CNS. The relative cell proliferation (RCP) and cytotoxicity grades exhibited no marked differences (P >0.05) between the cancer cells cultured with DMEM and those with PLA-PCL scaffold extract over time. Proteomic analysis identified 127 differentially expressed proteins (DEPs) in HIV-associated CRC cells co-cultured with LAF-PLA-PCL CNS, and Gene Ontology (GO) protein and KEGG pathway enrichment analysis (KEGG analysis) revealed that the LAF-PLA-PCL NCS could affect the cell cycle (CC) of HIV-associated CRC cells. In conclusion, the PLA-PCL NCS exhibited good compatibility, crystallinity, and biological activity, while the LAF-PLA-PCL NCS showed the potential to inhibit cell proliferation by affecting the CC.

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