3 research outputs found
Hyperspectral Stimulated Raman Scattering Microscopy Unravels Aberrant Accumulation of Saturated Fat in Human Liver Cancer
Lipid
metabolism is dysregulated in human cancers. The analytical
tools that could identify and quantitatively map metabolites in unprocessed
human tissues with submicrometer resolution are highly desired. Here,
we implemented analytical hyperspectral stimulated Raman scattering
microscopy to map the lipid metabolites in situ in normal and cancerous
liver tissues from 24 patients. In contrast to the conventional wisdom
that unsaturated lipid accumulation enhances tumor cell survival and
proliferation, we unexpectedly visualized substantial amount of saturated
fat accumulated in cancerous liver tissues, which was not seen in
majority of their adjacent normal tissues. Further analysis by mass
spectrometry confirmed significant high levels of glyceryl tripalmitate
specifically in cancerous liver. These findings suggest that the aberrantly
accumulated saturated fat may have great potential to be a metabolic
biomarker for liver cancer
Stimulated Raman Scattering Microscopy Reveals Aberrant Triglyceride Accumulation in Lymphatic Metastasis of Papillary Thyroid Carcinoma
Lipid metabolic alterations are known to play a crucial
role in
cancer metastasis. As a key hub in lipid metabolism, intracellular
neutral lipid accumulation in lipid droplets (LDs) has become a signature
of aggressive human cancers. Nevertheless, it remains unclear whether
lipid accumulation displays distinctive features in metastatic lesions
compared to the primary ones. Here, we integrated multicolor stimulated
Raman scattering (SRS) imaging with confocal Raman spectroscopy on
the same platform to quantitatively analyze the amount and composition
of LDs in intact human thyroid tissues in situ without
any processing or labeling. Inspiringly, we found aberrant accumulation
of triglycerides (TGs) in lymphatic metastases but not in normal thyroid,
primary papillary thyroid carcinoma (PTC), or normal lymph node. In
addition, the unsaturation degree of unsaturated TGs was significantly
higher in the lymphatic metastases from patients diagnosed with late-stage
(T3/T4) PTC compared to those of patients diagnosed with early-stage
(T1/T2) PTC. Furthermore, both public sequencing data analysis and
our RNA-seq transcriptomic experiment showed significantly higher
expression of alcohol dehydrogenase-1B (ADH1B), which is critical
to lipid uptake and transport, in lymphatic metastases relative to
the primary ones. In summary, these findings unravel the lipid accumulation
as a novel marker and therapeutic target for PTC lymphatic metastasis
that has a poor response to the regular radioactive iodine therapy
Caffeic Acid Phenethyl Ester, a Major Component of Propolis, Suppresses High Fat Diet-Induced Obesity through Inhibiting Adipogenesis at the Mitotic Clonal Expansion Stage
In the present study, we aimed to
investigate the antiobesity effect
of CAPE in vivo, and the mechanism by which CAPE regulates body weight
in vitro. To confirm the antiobesity effect of CAPE in vivo, mice
were fed with a high fat diet (HFD) with different concentrations
of CAPE for 5 weeks. CAPE significantly reduced body weight gain and
epididymal fat mass in obese mice fed a HFD. In accordance with in
vivo results, Oil red O staining results showed that CAPE significantly
suppressed MDI-induced adipogenesis of 3T3-L1 preadipocytes. FACS
analysis results showed that CAPE delayed MDI-stimulated cell cycle
progression, thereby contributing to inhibit mitotic clonal expansion
(MCE), which is a prerequisite step for adipogenesis. Also, CAPE regulated
the expression of cyclin D1 and the phosphorylation of ERK and Akt,
which are upstream of cyclin D1. These results suggest that CAPE exerts
an antiobesity effect in vivo, presumably through inhibiting adipogenesis
at an early stage of adipogenesis