Lipids represent a large family of compounds with highly
diverse
structures that are involved in complex biological processes. A photocatalytic
technique of on-tissue epoxidation of C=C double bonds has been developed
for in situ mass spectrometric identification and spatial imaging
of positional isomers of lipids. It is based on the plasmonic hot-electron
transfer from irradiated gold nanowires to redox-active organic matrix
compounds that undergo bond cleavages and generate hydroxyl radicals
in nanoseconds. Intermediate radical anions and negative fragment
ions have been unambiguously identified. Under the irradiation of
a pulsed laser of the third harmonic of Nd3+:YAG (355 nm),
the hydroxyl radical-driven epoxidation of unsaturated lipids with
different numbers of C=C bonds can be completed in nanoseconds with
high yields of up to 95%. Locations of C=C bonds were recognized with
diagnostic fragment ions that were produced by either collision with
an inert gas or auto-fragmentation resulting from the impact of energetic
hot electrons and vibrational excitation. This technique has been
applied to the analysis of breast cancer tissues of mice models without
extensive sample processes. It was experimentally demonstrated that
C=C bonds may be formed at different positions of not only regular
mono- or poly-unsaturated fatty acids but also other odd-numbered
long-chain fatty acids.
Background
The incidence of papillary thyroid cancer (PTC) has increased rapidly in recent decades, and tumor progression events are common in PTC. The purpose of our study is to identify the differentially expressed genes (DEGs) correlated with PTC progression and investigate the function of PDZK1IP1 in PTC.
Methods
We first analyzed DEGs associated with PTC progression between paired PTC and normal thyroid tissues in three GEO datasets (GSE29265, GSE33630 and GSE60542) and TCGA database. Data from TCGA database and our institution were utilized to explore the relationship between PDZK1IP1 expression and clinicopathological characteristics of PTC. The CCK8 cell proliferation assay, clone formation assay, flow cytometry assay and the xenograft model were used to investigate the function of PDZK1IP1 in PTC.
Results
39 DEGs associated with PTC progression were identified, in which only PDZK1IP1 was upregulated in PTC tissue at both mRNA and protein levels. Besides, we found that high expression of PDZK1IP1 in TCGA database was associated with poor progression-free survival, extrathyroidal extension, high stage, tall cell variant and BRAF V600E mutation of the PTC (P<0.001). In our collected samples, high expression of PDZK1IP1 was only related to lymph node metastasis (P<0.05). Overexpression of PDZK1IP1 significantly promoted proliferation and inhibited apoptosis of PTC cells. Knockdown of PDZK1IP1 significantly inhibited proliferation, promoted apoptosis, and prevented xenograft formation of PTC cells.
Conclusion
PDZK1IP1 is an oncogene for tumorigenesis and development of PTC and might be a potential therapeutic target.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.