In Situ Synthesis of CuS Nanoparticle-Doped Poly(<i>N</i>‑isopropylacrylamide)-Based Microgels for Near-Infrared Triggered Photothermal Therapy

Poly­(<i>N</i>-isopropylacrylamide)-<i>co</i>-(acrylic acid) (pNIPAm-<i>co</i>-AAc) microgels incorporated with CuS nanoparticles (CuSNPs) were synthesized and employed for near-infrared (NIR) triggered photothermal killing of cancer cells. Cu²⁺ was enriched in the microgels through deprotonation of the pNIPAm-<i>co</i>-AAc microgels at high solution pH. CuSNPs were subsequently generated within the pNIPAm-<i>co</i>-AAc microgels upon exposure to heat and S^2–. The solution of hybrid microgels showed an absorption peak in the NIR region (∼1000 nm). After demonstrating that the hybrid microgels were not cytotoxic, we showed that NIR excitation of the hybrid microgels could be used to kill HeLa cells. Almost 90% of the HeLa cells were killed when incubated with 400 μg/mL of the hybrid microgels and exposed to 808 nm laser light with a power density of 2 W/cm² for 10 min. While these materials show promise for photothermal therapy, they can also be incorporated into a hydrogel matrix that can be triggered to release small molecule drugs upon exposure to NIR wavelengths

The lncRNA RHPN1-AS1 downregulation promotes gefitinib resistance by targeting miR-299-3p/TNFSF12 pathway in NSCLC

<p>Although epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) gefitinib has exhibited notable clinical efficacy in non-small cell lung cancer (NSCLC) patients. However, its therapeutic efficacy is ultimately limited by the development of gefitinib resistance. The present study aimed to investigate the effects of the long non-coding RNA, RHPN1-AS1 on gefitinib resistance in NSCLC and explore the underlying mechanisms. In this study, RHPN1-AS1 was observed to be downregulated in gefitinib resistant patients and NSCLC cell lines. Besides, decreased expression of RHPN1-AS1 was found to be associated with poor prognosis of NSCLC patients. RHPN1-AS1 knockdown conferred gefitinib resistance to gefitinib sensitive NSCLC cells, whereas the overexpression of RHPN1-AS1 sensitized gefitinib resistant NSCLC cells to gefitinib treatment. Mechanistically, RHPN1-AS1 was found to positively regulate the expression of TNFSF12 by directly interacting with miR-299-3p. Collectively, RHPN1-AS1 modulates gefitinib resistance through miR-299-3p/TNFSF12 pathway in NSCLC. Our findings indicate that RHPN1-AS1 may serve as not only a prognostic biomarker for gefitinib resistance but also as a promising therapeutic biomarker and target for the treatment of NSCLC patients.</p