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Nucleus Near-Infrared (nNIR) Irradiation of Single A549 Cells Induces DNA Damage and Activates EGFR Leading to Mitochondrial Fission

為了解決X trail e:power 試駕的問題，作者MOMOH GBETUWA 這樣論述：

Abstract Background: There has been great interest in identifying the biological substrate for light-cell interaction and their relations to cancer treatment. In our study, a single cell nuclear NIR (nNIR) and cytosol exposed NIR has been used to determine for the first-time mitochondria fragmentat

ion count (MFC) to compare NIR effect on subcellular cells. Near infra-red (NIR) possesses less light scattering and absorption in biological tissues it has a biological window that bears a very small photodamage and thus possesses a deep tissue penetration depth. Aim: To evaluate near-infrared (NIR

) laser focused into the nucleus (nNIR) or cytoplasm (cNIR) of a single living cell by a high numerical aperture condenser to dissect the novel role of cell nucleus in mediating NIR effects on mitochondrial dynamics of A549 non-small cell lung cancer cells.Materials and Methods: Cultured 150 single

cell of A549 nucleus and cytosol were incubated with 0.3 μM mitotracker green for 30 min washed with PBS, imaged control cell then treated with 224.02 J/cm2 NIR for 10 s and cells imaged at different time points of 1, 5, 10, 15 and 20 min. A549 cells were treated with conjugated 100 nM FND-EGF and i

ncubated with PD153035, caffeine and cetuximab for 1 h, and imaged cells. Results: Our analysis showed nNIR, but not cNIR, triggered mitochondrial fission in 10 minutes. On the contrast, the fission/fusion balance of mitochondria directly exposed to cNIR does not change. While the same phenomenon is

also triggered by single molecular interactions between epidermal growth factor (EGF) and its receptor EGFR, pharmacological studies with cetuximab, PD153035 and caffeine suggest EGF signaling crosstalk to DNA damaging response to mediate rapid mitochondrial fission as a result of nNIR irradiation.

These results suggest that nuclear DNA integrity is a novel biological target for cellular response to NIR. Conclusions: These results suggest that nuclear DNA integrity is a novel biological target for cellular response to NIR. Keywords: Keywords: near infrared (NIR), epidermal growth factor recep

tor (EGFR), mitochondrial fragmentation count (MFC), mitochondrial dynamic, cetuximab, caffeine.

The Biological Function of Artemisia Santolinifolia as Anticancer Agent in NSCLC.

為了解決X trail e:power 試駕的問題，作者UYANGA BATBOLD 這樣論述：

Chemotherapy is currently one of the main modes commonly used in NSCLC treatment. Despite of toxicity and the development of chemodrug resistance, conventional chemotherapy endures as an essential segment of lung cancer management. Consequently, exploring a new alternative treatment for cancer ther

apy is needed. The genus Artemisia is composed of over 500 species, extracts of which have been mentioned as traditional remedies for controlling various maladies. However, not much is scientifically validated about how Artemisia santolinifolia (AS) might affect cancer cell proliferation. Our projec

t aimed to discover the prospective antitumor property of A.santolinifolia in non-small cell lung cancer (NSCLC) and the molecular mechanisms behind it. The effects of AS alone or merged with standard chemo drugs (such as Docetaxel, DTX) on cell feasibility were evaluated using sulforhodamine B (SRB

) assay. The 50% inhibitory concentrations (IC50) of AS and combination potencies of AS with DTX were assessed based on cell cytotoxicity results in two different NSCLC cell lines: A549 and H23. Results showed AS inhibited the growth of both A549 and H23 cells with IC50 of 206.6 and 213.4 µg/mL, res

pectively. The morphological observation and flow cytometry analysis showed that AS selectively induced different features of cell death in A549 and H23 cells. The phospholipid hydroperoxide glutathione peroxidase (GPX4) protein expression level, reaction oxygen species (ROS) generation and lipid pe

roxidation, which are all characteristic markers of iron-dependent cell death ferroptosis, were amended by AS predominately in A549 with the most alteration rate in the co-treatment group but similar effect was not observed in H23. Accordingly, above result suggests that AS possessed a chemosensitiz

ing effect via induction of ferroptosis in A549 cells. Contrarily, AS enhanced the effect of DTX- induced caspase-3 cleavage and accumulation of apoptosis cells in flow cytometry analysis, indicating caspase-dependent apoptosis was primarily involved in AS-induced additive effect selectively in H23

cells. Further investigations identified that AS could dual-selectively target Nuclear factor-E2-related factor 2 (NRF2) regulator, which was before reported to exert opposing effects upon activation or suppression. Nonetheless, despite triggering different kinds of cell death, the synergistic effec

t of AS merged with DTX was tightly connected with coadjutant suppression of oncogenesis signaling molecule STAT3 in both cell lines, accompanied with inhibition of prosurvival protein survivin, which plays a pivotal role in the STAT3 molecular pathway.This research indicated, AS could activate DTX-

induced cancer cell apoptosis with theinvolvement of inhibition of substantial prosurvival proteins' expressions and oxidative damage in A549 as its possible mechanism of action in iron-dependent cell death, while in contrast, activation of apoptosis-linked proteins in H23 cells triggering a differe

nt type of cell death. results highlight that AS could be an adjunctive pharmacologic therapeutic alternative when combined with a standard chemo drug in the management of patients with lung cancer.