echemi logo
Product
  • Product
  • Supplier
  • Inquiry
    Home > Biochemistry News > Biotechnology News > WE-PM10 promotes the molecular mechanism of cell metastasis in lung cancer and screens the main toxic components.

    WE-PM10 promotes the molecular mechanism of cell metastasis in lung cancer and screens the main toxic components.

    • Last Update: 2020-08-09
    • Source: Internet
    • Author: User
    Search more information of high quality chemicals, good prices and reliable suppliers, visit www.echemi.com
    Atmospheric particulate matter (Ambient particulate matter, PM) is the primary pollutant affecting urban air quality.
    a large number of epidemiological and toxicological studies have confirmed that PM can carry bacteria, viruses, metals, acidic oxides, organic pollutants and other harmful substances into the body, the respiratory system has a strong stimulating and sensitization effect, inducing chronic obstructive pulmonary disease, bronchitis, asthma and other chronic respiratory diseases, and even aggravating the development of lung cancer and malignant metastasis.
    the Environmental Medicine and Molecular Toxicology Research Group of the Institute of Urban Environment of the Chinese Academy of Sciences (Dong Sijun Team) and the Peking University School of Urban and Environmental College, Professor Tao Wei research team, collected the Beijing Autumn PM10, extracted water-soluble components (WE-PM10), and used the gene regulatory network of microRNA-mediated to study the molecular mechanism of WE-PM10 to promote cell transfer of lung cancer and screen the main toxic components.
    results showed that we-PM10 exposure led to reduced miR-26a expression in human non-small cell lung cancer cell line (A549), increased expression of Lin-28 homologous (LIN28B) and leukion-6 (IL6), signal-conductive and transcription-activator 3 (STAT3) activation, which ultimately promoted the translioscopy of A549 cells and enhanced its migration and invasion.
    naked mouse tumor experiment further confirmed that WE-PM10 can significantly enhance the tumor capacity in lung cancer cells.
    Based on the use of bioinformatics to predict the presence of junction sites of miR-26a on 3'UTR of LIN28B and IL6, the team used a cell model of the expression of the miR-26a difference to determine the direct regulation of miR-26a to predict LIN28B and confirmed that we-PM10 promotes a549 cell metastasis by miR-26a-LIN28B/IL6.
    it is worth noting that PM10 is a mixture of chemicalsubstances, and pm10 from different sources can vary widely due to formation conditions, time and space.
    PM10's health hazards mainly come from the toxic components of its load.
    , the refore, the study also used cation exchange resin chelation to remove the metal in WE-PM10, the results obviously interfered with WE-PM10 induced lung cancer cells inflammatory response and invasive metastasis, confirmed that atmospheric particles in the metal may be the key toxic component to promote lung cancer cell metastasis.
    the above findings were published in Archives of Toxicology (Archives of Toxicology, 2018, 92:1023-1035) with the title of MiR-26a functions as a tha ath-bound metal-triggered cancer cell metastasis by targeting LIN28B-IL6-STAT3 axis.
    Lu Yanyang is the first author, Lin Yi and Dong Sijun are co-authors.
    the study was supported by projects such as the National Natural Science Foundation of China (41390240, 21677140, 21477124) and the Chinese Academy of Sciences Youth Innovation Promotion Association (2017349).
    .
    This article is an English version of an article which is originally in the Chinese language on echemi.com and is provided for information purposes only. This website makes no representation or warranty of any kind, either expressed or implied, as to the accuracy, completeness ownership or reliability of the article or any translations thereof. If you have any concerns or complaints relating to the article, please send an email, providing a detailed description of the concern or complaint, to service@echemi.com. A staff member will contact you within 5 working days. Once verified, infringing content will be removed immediately.

    Contact Us

    The source of this page with content of products and services is from Internet, which doesn't represent ECHEMI's opinion. If you have any queries, please write to service@echemi.com. It will be replied within 5 days.

    Moreover, if you find any instances of plagiarism from the page, please send email to service@echemi.com with relevant evidence.