Excited State Kinetics of Benzo[a]pyrene Is Affected by Oxygen and DNA.

Benzo[a]pyrene is a widespread environmental pollutant and a strong carcinogen. It is important to understand its bio-toxicity and degradation mechanism. Herein, we studied the excited state dynamics of benzo[a]pyrene by using time-resolved fluorescence and transient absorption spectroscopic techniques. For the first time, it is identified that benzo[a]pyrene in its singlet excited state could react with oxygen, resulting in fluorescence quenching. Additionally, effective intersystem crossing can occur from its singlet state to the triplet state. Furthermore, the interaction between the excited benzo[a]pyrene and ct-DNA can be observed directly and charge transfer between benzo[a]pyrene and ct-DNA may be the reason. These results lay a foundation for further understanding of the carcinogenic mechanism of benzo[a]pyrene and provide insight into the photo-degradation mechanism of this molecule.

LncRNA highly upregulated in liver cancer regulates imatinib resistance in chronic myeloid leukemia via the miR-150-5p/MCL1 axis.

Chronic myeloid leukemia (CML) is a type of myeloproliferative neoplasm. Aberrant expression of long noncoding RNA highly upregulated in liver cancer (HULC) has been implicated in tumor progression, including CML. This study aimed to investigate the role of HULC in CML. The levels of HULC, miR-150-5p and myeloid cell leukemia 1 (MCL1) were examined by quantitative real-time PCR or western blot assay. Cell counting kit-8 assay was used to detect cell viability and half inhibition concentration. Cell apoptosis was monitored by flow cytometry and western blot. The interaction among HULC, miR-150-5p and MCL1 was validated by dual-luciferase reporter assay. The expression of phosphatidylinositol 3-kinase (PI3K), protein kinase B (AKT) and phosphorylation-AKT was evaluated using western blot assay. HULC and MCL1 were upregulated, whereas miR-150-5p was downregulated in bone marrow mononuclear cells of CML patients and CML cells. HULC overexpression increased imatinib resistance in K562 cells, and HULC depletion enhanced imatinib sensitivity in imatinib-resistant cells (K562-R). Mechanically, HULC was a sponge of miR-150-5p. HULC contributed to imatinib resistance through regulation of miR-150-5p. MCL1 bound to miR-150-5p and reversed the effect of HULC on imatinib resistance. HULC regulated the PI3K/AKT pathway via the miR-150-5p/MCL1 axis. These findings indicated that HULC enhanced imatinib resistance in CML by modulating the miR-150-5p/MCL1 axis, providing a promising biomarker for CML.