PIK3CB promotes oesophageal cancer proliferation through the PI3K/AKT/mTOR signalling axis

Abstract

PIK3CB is abnormally expressed in various carcinomas and affects the proliferation, invasion and drug resistance of cancer cells. However, its role in oesophageal squamous cell carcinoma (ESCC) is still unclear. In this study, PIK3CB was found to be highly expressed in ESCC tissues and cells and positively correlated with the poor prognosis of ESCC. Silencing PIK3CB inhibited the proliferation of ESCC cells, arrested the cell cycle, and promoted apoptosis. Mechanistic studies showed that the tumour-promoting effect of PIK3CB was achieved through PI3K/AKT/mTOR signalling pathway activation. Moreover, the high PIK3CB expression level in ESCC may be closely associated with the hypomethylation status of the gene promoter. In conclusion, PIK3CB promotes ESCC by activating the PI3K/AKT/mTOR signalling axis. PIK3CB may be a potential target in ESCC.

Isolation of proteins on chromatin (iPOC) reveals signaling pathway-dependent alterations in the DNA-bound proteome

“…In order to boost the enrichment efficiency and the signal to noise, here we have optimized a number of key steps in the iPOC sample preparation procedure with regard to EdU concentration, prS beads-to-input ratio, time for decrosslinking, protein digestion, and peptide desalting strategies, thereby establishing the optimal working conditions to study the DNAbound proteome. So far, the regulation of signaling cascades is often investigated at the level of protein phosphorylation, either using phospho-specific antibodies in either ELISA or western blots to confirm pathway activation [43], or by phospho-proteomics to investigate kinase-dependent signaling networks in a more unbiased and integrative fashion [44]. Despite their power and wide-spread use, these approaches primarily capture upstream events occurring in the cytosol upon pathway activation, while they are not designed to describe downstream consequences in chromatin, representing an important regulatory layer that mediates signaling output (i.e.…”

“…So far, the regulation of signaling cascades is often investigated at the level of protein phosphorylation, either using phospho-specific antibodies in either ELISA or western blots to confirm pathway activation [43], or by phospho-proteomics to investigate kinase-dependent signaling networks in a more unbiased and integrative fashion [44]. Despite their power and wide-spread use, these approaches primarily capture upstream events occurring in the cytosol upon pathway activation, while they are not designed to describe downstream consequences in chromatin, representing an important regulatory layer that mediates signaling output (i.e.…”

Interplay of miR-542, miR-126, miR-143 and miR-26b withPI3K-AKT is a diagnostic signal and putative regulatory target in HPV-Positive Cervical Cancer

“…PIK3CB subunit of PI3K and AKT1 isoform of Akt are important genes in the PI3K-Akt signaling pathway(Schüller et al 2008;Xu et al 2022). AKT1 encodes the RAC-alpha serine/threonine-protein kinase oncogene(Schüller et al 2008) and upregulation of PIK3CB induces cancer formation(Xu et al 2022). These observations support the idea that these miRNAs have the potential to inhibit the PI3K-AKT pathway.…”