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    Home > Active Ingredient News > Antitumor Therapy > Cell Death Dis:lncRNA LRRC75A-AS1 promotes the development of triple negative breast cancer.

    Cell Death Dis:lncRNA LRRC75A-AS1 promotes the development of triple negative breast cancer.

    • Last Update: 2020-09-23
    • Source: Internet
    • Author: User
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    Breast cancer (BC) is one of the most common malignant tumors in women and is the leading cause of death among women worldwide, accounting for about 6.6% of cancer deaths worldwide.
    -negative breast cancer (TNBC) is one of the most serious subtypes of breast cancer, characterized by a lack of expression of estrogen receptors and progesterone receptors.
    chemotherapy is currently the preferred treatment for TNBC patients.
    long non-coding RNA (lncRNA) is a set of non-coding RNA that is longer than 200 nucleotides.
    growing evidence that lncRNA plays a regulatory role in a variety of cancers, including TNBC.
    previous studies have found that the new lncRNA LRRC75A-AS1 (also known as SNHG29) located on chromosome 17p11.2 has carcinogenic properties.
    BAALC as a common carcinogenic gene for acute granulocytic leukemia (AML), the researchers previously found a significant increase in BAALC expression levels in TNBC tissues and cells.
    the study explores the role of BAALC in TNBC and the regulatory role of the LRRC75A-AS1/miR-380-3p/BAALC signal path in TNBC.
    study showed that BAALC promotes cell proliferation, invasion, and endocal-interstrate transformation (EMT) processes, and inhibits TNBC apoptosis.
    further studies have found that LRRC75A-AS1 can act as a molecular sponge of miR-380-3p, competitively binding miR-380-3p and inhibiting its expression, while miR-380-3p is the upstream miRNA of BAALC in TNBC cells, indicating that LRRC75A-AS1 can negatively regulate the expression of miR-380-3p and is positively regulating BAALC expression.
    Reescue rescue experiment also showed that LRRC75A-AS1 in TNBC was able to promote cell proliferation, invasion, and EMT processes by targeting miR-380-3p/BAALC pathps.
    results show that LRRC75A-AS1/miR-380-3p/BAALC, a new regulatory network, can accelerate the development of TNBC, and reveal that the signal path may be a new target for TNBC treatment.
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